A BLOOD PRESSURE regulating system of interacting components that include RENIN; ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; ANGIOTENSIN I; ANGIOTENSIN II; and angiotensinase. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I. Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II, an extremely powerful vasoconstrictor. Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure. In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney. Angiotensin-converting enzyme also breaks down BRADYKININ, a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM.
A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC 3.4.99.19.
An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.
An angiotensin receptor subtype that is expressed at high levels in a variety of adult tissues including the CARDIOVASCULAR SYSTEM, the KIDNEY, the ENDOCRINE SYSTEM and the NERVOUS SYSTEM. Activation of the type 1 angiotensin receptor causes VASOCONSTRICTION and sodium retention.
An alpha-globulin of about 453 amino acids, depending on the species. It is produced by the liver and secreted into blood circulation. Angiotensinogen is the inactive precursor of natural angiotensins. Upon successive enzyme cleavages, angiotensinogen yields angiotensin I, II, and III with amino acids numbered at 10, 8, and 7, respectively.
Oligopeptides which are important in the regulation of blood pressure (VASOCONSTRICTION) and fluid homeostasis via the RENIN-ANGIOTENSIN SYSTEM. These include angiotensins derived naturally from precursor ANGIOTENSINOGEN, and those synthesized.
A decapeptide that is cleaved from precursor angiotensinogen by RENIN. Angiotensin I has limited biological activity. It is converted to angiotensin II, a potent vasoconstrictor, after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME.
A peptidyl-dipeptidase that catalyzes the release of a C-terminal dipeptide, -Xaa-*-Xbb-Xcc, when neither Xaa nor Xbb is Pro. It is a Cl(-)-dependent, zinc glycoprotein that is generally membrane-bound and active at neutral pH. It may also have endopeptidase activity on some substrates. (From Enzyme Nomenclature, 1992) EC 3.4.15.1.
A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility.
An angiotensin receptor subtype that is expressed at high levels in fetal tissues. Many effects of the angiotensin type 2 receptor such as VASODILATION and sodium loss are the opposite of that of the ANGIOTENSIN TYPE 1 RECEPTOR.
Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells.
Agents that antagonize ANGIOTENSIN II TYPE 1 RECEPTOR. Included are ANGIOTENSIN II analogs such as SARALASIN and biphenylimidazoles such as LOSARTAN. Some are used as ANTIHYPERTENSIVE AGENTS.
Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.
An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
An angiotensin-converting enzyme inhibitor that is used to treat HYPERTENSION and HEART FAILURE.
A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
Tetrazoles are heterocyclic organic compounds containing a 1,3,5-triazole ring with an additional nitrogen atom, often used in pharmaceuticals as bioisosteres for carboxylic acid groups due to their isoelectronic nature and similar hydrogen bonding capabilities.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.
KIDNEY injuries associated with diabetes mellitus and affecting KIDNEY GLOMERULUS; ARTERIOLES; KIDNEY TUBULES; and the interstitium. Clinical signs include persistent PROTEINURIA, from microalbuminuria progressing to ALBUMINURIA of greater than 300 mg/24 h, leading to reduced GLOMERULAR FILTRATION RATE and END-STAGE RENAL DISEASE.
An ANGIOTENSIN II analog which acts as a highly specific inhibitor of ANGIOTENSIN TYPE 1 RECEPTOR.
The presence of albumin in the urine, an indicator of KIDNEY DISEASES.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
One of the ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE inhibitors), orally active, that has been used in the treatment of hypertension and congestive heart failure.
A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.
Biphenyl compounds are organic substances consisting of two phenyl rings connected by a single covalent bond, and can exhibit various properties and uses, including as intermediates in chemical synthesis, components in plastics and dyes, and as additives in fuels.
A heptapeptide formed from ANGIOTENSIN II after the removal of an amino acid at the N-terminal by AMINOPEPTIDASE A. Angiotensin III has the same efficacy as ANGIOTENSIN II in promoting ALDOSTERONE secretion and modifying renal blood flow, but less vasopressor activity (about 40%).
Compounds based on fumaric acid.
Elements of limited time intervals, contributing to particular results or situations.
Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).
Compounds with a BENZENE fused to IMIDAZOLES.
Agents that antagonize the ANGIOTENSIN II TYPE 2 RECEPTOR.
A long-acting angiotensin-converting enzyme inhibitor. It is a prodrug that is transformed in the liver to its active metabolite ramiprilat.
The circulation of the BLOOD through the vessels of the KIDNEY.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
An octapeptide analog of angiotensin II (bovine) with amino acids 1 and 8 replaced with sarcosine and alanine, respectively. It is a highly specific competitive inhibitor of angiotensin II that is used in the diagnosis of HYPERTENSION.
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Drugs used to cause constriction of the blood vessels.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
Persistent high BLOOD PRESSURE due to KIDNEY DISEASES, such as those involving the renal parenchyma, the renal vasculature, or tumors that secrete RENIN.
A diet which contains very little sodium chloride. It is prescribed by some for hypertension and for edematous states. (Dorland, 27th ed)
A synthetic nonapeptide (Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro) which is identical to the peptide from the venom of the snake, Bothrops jararaca. It inhibits kininase II and ANGIOTENSIN I and has been proposed as an antihypertensive agent.
The octapeptide amide of bovine angiotensin II used to increase blood pressure by vasoconstriction.
A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.
The active metabolite of ENALAPRIL and a potent intravenously administered angiotensin-converting enzyme inhibitor. It is an effective agent for the treatment of essential hypertension and has beneficial hemodynamic effects in heart failure. The drug produces renal vasodilation with an increase in sodium excretion.
Hypertension due to RENAL ARTERY OBSTRUCTION or compression.
Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.
A strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR).
A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.
The relationship between the dose of an administered drug and the response of the organism to the drug.
The nonstriated involuntary muscle tissue of blood vessels.
A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
A branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway.
The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.
Excision of kidney.
A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.
A family of neutral serine proteases with CHYMOTRYPSIN-like activity. Chymases are primarily found in the SECRETORY GRANULES of MAST CELLS and are released during mast cell degranulation.
A pair of glands located at the cranial pole of each of the two KIDNEYS. Each adrenal gland is composed of two distinct endocrine tissues with separate embryonic origins, the ADRENAL CORTEX producing STEROIDS and the ADRENAL MEDULLA producing NEUROTRANSMITTERS.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
Enlargement of the HEART, usually indicated by a cardiothoracic ratio above 0.50. Heart enlargement may involve the right, the left, or both HEART VENTRICLES or HEART ATRIA. Cardiomegaly is a nonspecific symptom seen in patients with chronic systolic heart failure (HEART FAILURE) or several forms of CARDIOMYOPATHIES.
The main trunk of the systemic arteries.
Organic compounds containing the -CO-NH2 radical. Amides are derived from acids by replacement of -OH by -NH2 or from ammonia by the replacement of H by an acyl group. (From Grant & Hackh's Chemical Dictionary, 5th ed)
A direct-acting vasodilator that is used as an antihypertensive agent.
Sodium excretion by URINATION.

Insulin-like growth factor-1 induces Mdm2 and down-regulates p53, attenuating the myocyte renin-angiotensin system and stretch-mediated apoptosis. (1/2490)

Insulin-like growth factor (IGF)-1 inhibits apoptosis, but its mechanism is unknown. Myocyte stretching activates p53 and p53-dependent genes, leading to the formation of angiotensin II (Ang II) and apoptosis. Therefore, this in vitro system was used to determine whether IGF-1 interfered with p53 function and the local renin-angiotensin system (RAS), decreasing stretch-induced cell death. A single dose of 200 ng/ml IGF-1 at the time of stretching decreased myocyte apoptosis 43% and 61% at 6 and 20 hours. Ang II concentration was reduced 52% at 20 hours. Additionally, p53 DNA binding to angiotensinogen (Aogen), AT1 receptor, and Bax was markedly down-regulated by IGF-1 via the induction of Mdm2 and the formation of Mdm2-p53 complexes. Concurrently, the quantity of p53, Aogen, renin, AT1 receptor, and Bax was reduced in stretched myocytes exposed to IGF-1. Conversely, Bcl-2 and the Bcl-2-to-Bax protein ratio increased. The effects of IGF-1 on cell death, Ang II synthesis, and Bax protein were the consequence of Mdm2-induced down-regulation of p53 function. In conclusion, the anti-apoptotic impact of IGF-1 on stretched myocytes was mediated by its capacity to depress p53 transcriptional activity, which limited Ang II formation and attenuated the susceptibility of myocytes to trigger their endogenous cell death pathway.  (+info)

Blocking angiotensin II ameliorates proteinuria and glomerular lesions in progressive mesangioproliferative glomerulonephritis. (2/2490)

BACKGROUND: The renin-angiotensin system is thought to be involved in the progression of glomerulonephritis (GN) into end-stage renal failure (ESRF) because of the observed renoprotective effects of angiotensin-converting enzyme inhibitors (ACEIs). However, ACEIs have pharmacological effects other than ACE inhibition that may help lower blood pressure and preserve glomerular structure. We previously reported a new animal model of progressive glomerulosclerosis induced by a single intravenous injection of an anti-Thy-1 monoclonal antibody, MoAb 1-22-3, in uninephrectomized rats. Using this new model of progressive GN, we examined the hypothesis that ACEIs prevent the progression to ESRF by modulating the effects of angiotensin II (Ang II) on the production of transforming growth factor-beta (TGF-beta) and extracellular matrix components. METHODS: We studied the effect of an ACEI (cilazapril) and an Ang II type 1 receptor antagonist (candesartan) on the clinical features and morphological lesions in the rat model previously reported. After 10 weeks of treatment with equihypotensive doses of cilazapril, cilazapril plus Hoe 140 (a bradykinin receptor B2 antagonist), candesartan, and hydralazine, we examined systolic blood pressure, urinary protein excretion, creatinine clearance, the glomerulosclerosis index, and the tubulointerstitial lesion index. We performed a semiquantitative evaluation of glomerular immunostaining for TGF-beta and collagen types I and III by immunofluorescence study and of these cortical mRNA levels by Northern blot analysis. RESULTS: Untreated rats developed massive proteinuria, renal dysfunction, and severe glomerular and tubulointerstitial injury, whereas uninephrectomized control rats did not. There was a significant increase in the levels of glomerular protein and cortical mRNA for TGF-beta and collagen types I and III in untreated rats. Cilazapril and candesartan prevented massive proteinuria, increased creatinine clearance, and ameliorated glomerular and tubulointerstitial injury. These drugs also reduced levels of glomerular protein and cortical mRNA for TGF-beta and collagen types I and III. Hoe 140 failed to blunt the renoprotective effect of cilazapril. Hydralazine did not exhibit a renoprotective effect. CONCLUSION: These results indicate that ACEIs prevent the progression to ESRF by modulating the effects of Ang II via Ang II type 1 receptor on the production of TGF-beta and collagen types I and III, as well as on intrarenal hemodynamics, but not by either increasing bradykinin activity or reducing blood pressure in this rat model of mesangial proliferative GN.  (+info)

Genetic determinants of diabetic nephropathy. (3/2490)

Diabetic nephropathy is the most serious complication of diabetes mellitus. Progression of the condition leads to end-stage renal failure, and other complications of diabetes are also common in this group of patients. The onset of overt albuminuria in a patient with diabetes heralds an increased risk of death, particularly from cardiovascular disease. There is considerable evidence to show that nephropathy is influenced by genetic factors. Epidemiological studies show that only a minority of patients with diabetes develop nephropathy irrespective of glycaemic control, suggesting that a subgroup of patients are at higher risk of nephropathy. Marked ethnic variation is observed, with nephropathy being more common in certain ethnic groups. Familial clustering of nephropathy is also observed. Parental history of hypertension, diabetes or cardiovascular disease appears to predispose to nephropathy in patients with diabetes. A number of methods are available to dissect polygenic disease: animal models, genetic association studies (case-control studies), affected sib-pair studies, discordant sib-pair studies and transmission distortion analysis. Most published work has been based on association studies. Association studies have shown conflicting results often due to small numbers of cases and controls, and poor phenotypic characterization. The angiotensin-converting enzyme gene insertion (I)/deletion (D) polymorphism has been studied in detail, but does not appear to be a strong risk marker for nephropathy. It does, however, appear to have a role in response to angiotensin-converting enzyme inhibition, with II homozygotes being the most responsive and DD homozygotes the least. A number of other genetic loci have also shown positive associations with nephropathy, including apolipoprotein E, heparan sulphate and aldose reductase. More recently, affected sib-pair analysis and discordant sib-pair analysis have suggested possible genetic loci on chromosomes 3, 7, 9, 12 and 20. These have yet to be reproduced in larger numbers of families, and the specific gene regions on these chromosomes remain elusive. The evidence presented in this review strongly supports the role of genetic factors in nephropathy. Detection of strong genetic risk markers for nephropathy will allow further insights into the pathogenesis of nephropathy, and possibly the development of novel therapeutic agents for its treatment. It will also allow preventive therapy to be directed at those patients with the greatest risk for development of diabetic nephropathy.  (+info)

Contribution of endothelin to renal vascular tone and autoregulation in the conscious dog. (4/2490)

Exogenous endothelin-1 (ET-1) is a strong vasoconstrictor in the canine kidney and causes a decrease in renal blood flow (RBF) by stimulating the ETA receptor subtype. The aim of the present study was to investigate the role of endogenously generated ET-1 in renal hemodynamics under physiological conditions. In six conscious foxhounds, the time course of the effects of the selective ETA receptor antagonist LU-135252 (10 mg/kg iv) on mean arterial blood pressure (MAP), heart rate (HR), RBF, and glomerular filtration rate (GFR), as well as its effects on renal autoregulation, were examined. LU-135252 increased RBF by 20% (from 270 +/- 21 to 323 +/- 41 ml/min, P < 0.05) and HR from 76 +/- 5 to 97 +/- 8 beats/min (P < 0. 05), but did not alter MAP, GFR, or autoregulation of RBF and GFR. Since a number of interactions between ET-1 and the renin-angiotensin system have been reported previously, experiments were repeated during angiotensin converting enzyme (ACE) inhibition by trandolaprilat (2 mg/kg iv). When ETA receptor blockade was combined with ACE inhibition, which by itself had no effects on renal hemodynamics, marked changes were observed: MAP decreased from 91 +/- 4 to 80 +/- 5 mmHg (P < 0.05), HR increased from 85 +/- 5 to 102 +/- 11 beats/min (P < 0.05), and RBF increased from 278 +/- 23 to 412 +/- 45 ml/min (P < 0.05). Despite a pronounced decrease in renal vascular resistance over the entire pressure range investigated (40-100 mmHg), the capacity of the kidneys to autoregulate RBF was not impaired. The GFR remained completely unaffected at all pressure levels. These results demonstrate that endogenously generated ET-1 contributes significantly to renal vascular tone but does not interfere with the mechanisms of renal autoregulation. If ETA receptors are blocked, then the vasoconstrictor effects of ET-1 in the kidney are compensated for to a large extent by an augmented influence of ANG II. Thus ET-1 and ANG II appear to constitute a major interrelated vasoconstrictor system in the control of RBF.  (+info)

Angiotensin II plays a pathogenic role in immune-mediated renal injury in mice. (5/2490)

Several lines of evidence show the importance of angiotensin II (AII) in renal injuries, especially when hemodynamic abnormalities are involved. To elucidate the role of AII in immune-mediated renal injury, we studied anti-glomerular basement membrane (GBM) nephritis in AII type 1a receptor (AT1a)-deficient homozygous (AT1a-/-) and wild-type (AT1a+/+) mice. A transient activation of the renin-angiotensin system (RAS) was observed in both groups of mice at around day 1. A renal expression of monocyte chemoattractant protein-1 (MCP-1) was transiently induced at six hours in both groups, which was then downregulated at day 1. In the AT1a+/+ mice, after RAS activation, the glomerular expression of MCP-1 was exacerbated at days 7 and 14. Thereafter, severe proteinuria developed, and the renal expressions of transforming growth factor-beta1 (TGF-beta1) and collagen type I increased, resulting in severe glomerulosclerosis and interstitial fibrosis. In contrast, glomerular expression of MCP-1, proteinuria, and tissue damage were markedly ameliorated in the AT1a-/- mice. Because this amelioration is likely due to the lack of AT1a, we can conclude that AII action, mediated by AT1a, plays a pathogenic role in anti-GBM nephritis, in which AII may contribute to the exacerbation of glomerular MCP-1 expression. These results suggest the involvement of AII in immune-mediated renal injuries.  (+info)

Mediation of humoral catecholamine secretion by the renin-angiotensin system in hypotensive rainbow trout (Oncorhynchus mykiss). (6/2490)

The individual contributions of, and potential interactions between, the renin-angiotensin system (RAS) and the humoral adrenergic stress response to blood pressure regulation were examined in rainbow trout. Intravenous injection of the smooth muscle relaxant, papaverine (10 mg/kg), elicited a transient decrease in dorsal aortic blood pressure (PDA) and systemic vascular resistance (RS), and significant increases in plasma angiotensin II (Ang II) and catecholamine concentrations. Blockade of alpha-adrenoceptors before papaverine treatment prevented PDA and RS recovery, had no effect on the increase in plasma catecholamines, and resulted in greater plasma Ang II concentrations. Administration of the angiotensin-converting enzyme inhibitor, lisinopril (10(-4) mol/kg), before papaverine treatment attenuated the increases in the plasma concentrations of Ang II, adrenaline, and noradrenaline by 90, 79, and 40%, respectively and also prevented PDA and RS recovery. By itself, lisinopril treatment caused a gradual and sustained decrease in PDA and RS, and reductions in basal plasma Ang II and adrenaline concentrations. Bolus injection of a catecholamine cocktail (4 nmol/kg noradrenaline plus 40 nmol/kg adrenaline) in the lisinopril+papaverine-treated trout, to supplement their circulating catecholamine concentrations and mimic those observed in fish treated only with papaverine, resulted in a temporary recovery in PDA and RS. These results indicate that the RAS and the acute humoral adrenergic response are both recruited during an acute hypotensive stress, and have important roles in the compensatory response to hypotension in rainbow trout. However, whereas the contribution of the RAS to PDA recovery is largely indirect and relies on an Ang II-mediated secretion of catecholamines, the contribution from the adrenergic system is direct and relies at least in part on plasma catecholamines.  (+info)

Angiotensin II attenuates renal cortical cyclooxygenase-2 expression. (7/2490)

We have previously shown that in rat renal cortex, cyclooxygenase-2 (COX-2) expression is localized to cTALH cells in the region of the macula densa, and that dietary salt restriction increases COX-2 expression. Administration of the angiotensin converting inhibitor, captopril, further increased COX-2 mRNA and renal cortical COX-2 immunoreactivity, with the most pronounced expression in the macula densa. Administration of an AT1 receptor antagonist, losartan, also significantly increased cortical COX-2 mRNA expression and COX-2 immunoreactivity. Mutant mice homozygous for both Agtr1a and Agtr1b null mutations (Agtr1a-/-,Agtr1b-/-) demonstrated large increases in immunoreactive COX-2 expression inthe cTALH/macula densa. To determine whether increased COX-2expression in response to ACE inhibition mediated increases in renin production, rats were treated with captopril for one week with or without the specific COX-2 inhibitor, SC58236. Plasma renin activity increased significantly in the captropril group, and this increase was significantly inhibited by simultaneous treatment with SC58236. Thus, these studies indicated that angiotensin II inhibitors augment upregulation of renal cortical COX-2 in states of volume depletion, suggesting that negative feedback by the renin-angiotensin system modulates renal cortical COX-2 expression and that COX-2 is a mediator of increased renin production in response to inhibition of angiotension II production.  (+info)

Overexpression of insulin-like growth factor-1 attenuates the myocyte renin-angiotensin system in transgenic mice. (8/2490)

Constitutive overexpression of insulin-like growth factor-1 (IGF-1) in myocytes protects them from apoptosis and interferes with myocyte hypertrophy in the normal and pathological heart. Conversely, angiotensin II (Ang II) triggers cell death and promotes myocyte hypertrophy. Moreover, activation of p53 upregulates the cellular renin-angiotensin system (RAS). Therefore, IGF-1 overexpression in FVB.Igf+/- mice may downregulate the local RAS through the attenuation of p53 and p53-inducible genes. On this basis, p53 DNA binding activity to angiotensinogen (Aogen), bax, and the AT1 receptor was determined in left ventricular myocytes from FVB.Igf-/- and FVB.Igf+/- mice. The quantity of Bax, Bcl-2, Aogen, and AT1 receptor in these cells was evaluated. The presence of Mdm2-p53 complexes was also established. Finally, Ang II levels in myocytes were measured. Upregulation of IGF-1 in myocytes was associated with a protein-to-protein interaction between Mdm2 and p53, which attenuated p53 transcriptional activity for bax, Aogen, and AT1 receptor. Similarly, the amount of Bax, Aogen, and AT1 receptor proteins in these cells decreased. In contrast, the expression of Bcl-2 remained constant. The downregulation of Aogen in myocytes from FVB.Igf+/- mice was characterized by a reduction in Ang II. In conclusion, IGF-1 negatively influences the myocyte RAS through the upregulation of Mdm2 and its binding to p53. This may represent the molecular mechanism responsible for the effects of IGF-1 on cell viability and myocyte hypertrophy in the nonpathological and pathological heart in vivo.  (+info)

The Renin-Angiotensin System (RAS) is a complex hormonal system that regulates blood pressure, fluid and electrolyte balance, and vascular resistance. It plays a crucial role in the pathophysiology of hypertension, heart failure, and kidney diseases.

Here's a brief overview of how it works:

1. Renin is an enzyme that is released by the juxtaglomerular cells in the kidneys in response to decreased blood pressure or reduced salt delivery to the distal tubules.
2. Renin acts on a protein called angiotensinogen, which is produced by the liver, converting it into angiotensin I.
3. Angiotensin-converting enzyme (ACE), found in the lungs and other tissues, then converts angiotensin I into angiotensin II, a potent vasoconstrictor that narrows blood vessels and increases blood pressure.
4. Angiotensin II also stimulates the release of aldosterone from the adrenal glands, which promotes sodium and water reabsorption in the kidneys, further increasing blood volume and blood pressure.
5. Additionally, angiotensin II has direct effects on the heart, promoting hypertrophy and remodeling, which can contribute to heart failure.
6. The RAS can be modulated by various medications, such as ACE inhibitors, angiotensin receptor blockers (ARBs), and aldosterone antagonists, which are commonly used to treat hypertension, heart failure, and kidney diseases.

Renin is a medically recognized term and it is defined as:

"A protein (enzyme) that is produced and released by specialized cells (juxtaglomerular cells) in the kidney. Renin is a key component of the renin-angiotensin-aldosterone system (RAAS), which helps regulate blood pressure and fluid balance in the body.

When the kidney detects a decrease in blood pressure or a reduction in sodium levels, it releases renin into the bloodstream. Renin then acts on a protein called angiotensinogen, converting it to angiotensin I. Angiotensin-converting enzyme (ACE) subsequently converts angiotensin I to angiotensin II, which is a potent vasoconstrictor that narrows blood vessels and increases blood pressure.

Additionally, angiotensin II stimulates the adrenal glands to release aldosterone, a hormone that promotes sodium reabsorption in the kidneys and increases water retention, further raising blood pressure.

Therefore, renin plays a critical role in maintaining proper blood pressure and electrolyte balance in the body."

Angiotensin II is a potent vasoactive peptide hormone that plays a critical role in the renin-angiotensin-aldosterone system (RAAS), which is a crucial regulator of blood pressure and fluid balance in the body. It is formed from angiotensin I through the action of an enzyme called angiotensin-converting enzyme (ACE).

Angiotensin II has several physiological effects on various organs, including:

1. Vasoconstriction: Angiotensin II causes contraction of vascular smooth muscle, leading to an increase in peripheral vascular resistance and blood pressure.
2. Aldosterone release: Angiotensin II stimulates the adrenal glands to release aldosterone, a hormone that promotes sodium reabsorption and potassium excretion in the kidneys, thereby increasing water retention and blood volume.
3. Sympathetic nervous system activation: Angiotensin II activates the sympathetic nervous system, leading to increased heart rate and contractility, further contributing to an increase in blood pressure.
4. Thirst regulation: Angiotensin II stimulates the hypothalamus to increase thirst, promoting water intake and helping to maintain intravascular volume.
5. Cell growth and fibrosis: Angiotensin II has been implicated in various pathological processes, such as cell growth, proliferation, and fibrosis, which can contribute to the development of cardiovascular and renal diseases.

Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) are two classes of medications commonly used in clinical practice to target the RAAS by blocking the formation or action of angiotensin II, respectively. These drugs have been shown to be effective in managing hypertension, heart failure, and chronic kidney disease.

The Angiotensin II Receptor Type 1 (AT1 receptor) is a type of G protein-coupled receptor that binds and responds to the hormone angiotensin II, which plays a crucial role in the renin-angiotensin-aldosterone system (RAAS). The RAAS is a vital physiological mechanism that regulates blood pressure, fluid, and electrolyte balance.

The AT1 receptor is found in various tissues throughout the body, including the vascular smooth muscle cells, cardiac myocytes, adrenal glands, kidneys, and brain. When angiotensin II binds to the AT1 receptor, it activates a series of intracellular signaling pathways that lead to vasoconstriction, increased sodium and water reabsorption in the kidneys, and stimulation of aldosterone release from the adrenal glands. These effects ultimately result in an increase in blood pressure and fluid volume.

AT1 receptor antagonists, also known as angiotensin II receptor blockers (ARBs), are a class of drugs used to treat hypertension, heart failure, and other cardiovascular conditions. By blocking the AT1 receptor, these medications prevent angiotensin II from exerting its effects on the cardiovascular system, leading to vasodilation, decreased sodium and water reabsorption in the kidneys, and reduced aldosterone release. These actions ultimately result in a decrease in blood pressure and fluid volume.

Angiotensinogen is a protein that is produced mainly by the liver. It is the precursor to angiotensin I, which is a molecule that begins the process of constriction (narrowing) of blood vessels, leading to an increase in blood pressure. When angiotensinogen comes into contact with an enzyme called renin, it is cleaved into angiotensin I. Angiotensin-converting enzyme (ACE) then converts angiotensin I into angiotensin II, which is a potent vasoconstrictor and a key player in the body's regulation of blood pressure and fluid balance.

Angiotensinogen is an important component of the renin-angiotensin-aldosterone system (RAAS), which helps to regulate blood pressure and fluid balance by controlling the volume and flow of fluids in the body. Disorders of the RAAS can lead to high blood pressure, kidney disease, and other health problems.

Angiotensins are a group of hormones that play a crucial role in the body's cardiovascular system, particularly in regulating blood pressure and fluid balance. The most well-known angiotensins are Angiotensin I, Angiotensin II, and Angiotensin-(1-7).

Angiotensinogen is a protein produced mainly by the liver. When the body requires an increase in blood pressure, renin (an enzyme produced by the kidneys) cleaves angiotensinogen to form Angiotensin I. Then, another enzyme called angiotensin-converting enzyme (ACE), primarily found in the lungs, converts Angiotensin I into Angiotensin II.

Angiotensin II is a potent vasoconstrictor, causing blood vessels to narrow and increase blood pressure. It also stimulates the release of aldosterone from the adrenal glands, which leads to increased sodium reabsorption in the kidneys, further raising blood pressure and promoting fluid retention.

Angiotensin-(1-7) is a more recently discovered member of the angiotensin family. It has opposing effects to Angiotensin II, acting as a vasodilator and counterbalancing some of the negative consequences of Angiotensin II's actions.

Medications called ACE inhibitors and ARBs (angiotensin receptor blockers) are commonly used in clinical practice to target the renin-angiotensin system, lowering blood pressure and protecting against organ damage in various cardiovascular conditions.

Angiotensin I is a decapeptide (a peptide consisting of ten amino acids) that is generated by the action of an enzyme called renin on a protein called angiotensinogen. Renin cleaves angiotensinogen to produce angiotensin I, which is then converted to angiotensin II by the action of an enzyme called angiotensin-converting enzyme (ACE).

Angiotensin II is a potent vasoconstrictor, meaning it causes blood vessels to narrow and blood pressure to increase. It also stimulates the release of aldosterone from the adrenal glands, which leads to increased sodium and water reabsorption in the kidneys, further increasing blood volume and blood pressure.

Angiotensin I itself has little biological activity, but it is an important precursor to angiotensin II, which plays a key role in regulating blood pressure and fluid balance in the body.

Peptidyl-dipeptidase A is more commonly known as angiotensin-converting enzyme (ACE). It is a key enzyme in the renin-angiotensin-aldosterone system (RAAS), which regulates blood pressure and fluid balance.

ACE is a membrane-bound enzyme found primarily in the lungs, but also in other tissues such as the heart, kidneys, and blood vessels. It plays a crucial role in converting the inactive decapeptide angiotensin I into the potent vasoconstrictor octapeptide angiotensin II, which constricts blood vessels and increases blood pressure.

ACE also degrades the peptide bradykinin, which is involved in the regulation of blood flow and vascular permeability. By breaking down bradykinin, ACE helps to counteract its vasodilatory effects, thereby maintaining blood pressure homeostasis.

Inhibitors of ACE are widely used as medications for the treatment of hypertension, heart failure, and diabetic kidney disease, among other conditions. These drugs work by blocking the action of ACE, leading to decreased levels of angiotensin II and increased levels of bradykinin, which results in vasodilation, reduced blood pressure, and improved cardiovascular function.

Angiotensin-Converting Enzyme (ACE) inhibitors are a class of medications that are commonly used to treat various cardiovascular conditions, such as hypertension (high blood pressure), heart failure, and diabetic nephropathy (kidney damage in people with diabetes).

ACE inhibitors work by blocking the action of angiotensin-converting enzyme, an enzyme that converts the hormone angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor, meaning it narrows blood vessels and increases blood pressure. By inhibiting the conversion of angiotensin I to angiotensin II, ACE inhibitors cause blood vessels to relax and widen, which lowers blood pressure and reduces the workload on the heart.

Some examples of ACE inhibitors include captopril, enalapril, lisinopril, ramipril, and fosinopril. These medications are generally well-tolerated, but they can cause side effects such as cough, dizziness, headache, and elevated potassium levels in the blood. It is important for patients to follow their healthcare provider's instructions carefully when taking ACE inhibitors and to report any unusual symptoms or side effects promptly.

The Angiotensin II Receptor Type 2 (AT2R) is a type of G protein-coupled receptor that binds to the hormone angiotensin II, which plays a crucial role in the renin-angiotensin system (RAS), a vital component in regulating blood pressure and fluid balance.

The AT2R is expressed in various tissues, including the heart, blood vessels, kidneys, brain, and reproductive organs. When angiotensin II binds to the AT2R, it initiates several signaling pathways that can lead to vasodilation, anti-proliferation, anti-inflammation, and neuroprotection.

In contrast to the Angiotensin II Receptor Type 1 (AT1R), which is primarily associated with vasoconstriction, sodium retention, and fibrosis, AT2R activation has been shown to have protective effects in several pathological conditions, including hypertension, heart failure, atherosclerosis, and kidney disease.

However, the precise functions of AT2R are still being investigated, and its role in various physiological and pathophysiological processes may vary depending on the tissue type and context.

Angiotensin receptors are a type of G protein-coupled receptor that binds the angiotensin peptides, which are important components of the renin-angiotensin-aldosterone system (RAAS). The RAAS is a hormonal system that regulates blood pressure and fluid balance.

There are two main types of angiotensin receptors: AT1 and AT2. Activation of AT1 receptors leads to vasoconstriction, increased sodium and water reabsorption in the kidneys, and cell growth and proliferation. On the other hand, activation of AT2 receptors has opposite effects, such as vasodilation, natriuresis (increased excretion of sodium in urine), and anti-proliferative actions.

Angiotensin II is a potent activator of AT1 receptors, while angiotensin IV has high affinity for AT2 receptors. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are two classes of drugs that target the RAAS by blocking the formation or action of angiotensin II, leading to decreased activation of AT1 receptors and improved cardiovascular outcomes.

Angiotensin II Type 1 Receptor Blockers (ARBs) are a class of medications used to treat hypertension, heart failure, and protect against kidney damage in patients with diabetes. They work by blocking the action of angiotensin II, a hormone that causes blood vessels to constrict and blood pressure to increase, at its type 1 receptor. By blocking this effect, ARBs cause blood vessels to dilate, reducing blood pressure and decreasing the workload on the heart. Examples of ARBs include losartan, valsartan, irbesartan, and candesartan.

Angiotensin receptor antagonists (ARAs), also known as angiotensin II receptor blockers (ARBs), are a class of medications used to treat hypertension, heart failure, and protect against kidney damage in patients with diabetes. They work by blocking the action of angiotensin II, a potent vasoconstrictor and hormone that increases blood pressure and promotes tissue fibrosis. By blocking the binding of angiotensin II to its receptors, ARAs cause relaxation of blood vessels, decreased sodium and water retention, and reduced cardiac remodeling, ultimately leading to improved cardiovascular function and reduced risk of organ damage. Examples of ARAs include losartan, valsartan, irbesartan, and candesartan.

Losartan is an angiotensin II receptor blocker (ARB) medication that is primarily used to treat hypertension (high blood pressure), but can also be used to manage chronic heart failure and protect against kidney damage in patients with type 2 diabetes. It works by blocking the action of angiotensin II, a hormone that causes blood vessels to narrow and blood pressure to rise. By blocking this hormone's effects, losartan helps relax and widen blood vessels, making it easier for the heart to pump blood and reducing the workload on the cardiovascular system.

The medical definition of losartan is: "A synthetic angiotensin II receptor antagonist used in the treatment of hypertension, chronic heart failure, and diabetic nephropathy. It selectively blocks the binding of angiotensin II to the AT1 receptor, leading to vasodilation, decreased aldosterone secretion, and increased renin activity."

Enalapril is a medication that belongs to a class of drugs called angiotensin-converting enzyme (ACE) inhibitors. It works by blocking the action of a hormone in the body called angiotensin II, which causes blood vessels to narrow and tighten. By blocking this hormone, Enalapril helps relax and widen blood vessels, making it easier for the heart to pump blood and reducing the workload on the heart.

Enalapril is commonly used to treat high blood pressure (hypertension), congestive heart failure, and to improve survival after a heart attack. It may also be used to treat other conditions as determined by your doctor.

The medication comes in the form of tablets or capsules that are taken orally, usually once or twice a day with or without food. The dosage will depend on various factors such as the patient's age, weight, and medical condition. It is important to follow the instructions of your healthcare provider when taking Enalapril.

Like all medications, Enalapril can cause side effects, including dry cough, dizziness, headache, fatigue, and nausea. More serious side effects may include allergic reactions, kidney problems, and low blood pressure. If you experience any concerning symptoms while taking Enalapril, it is important to contact your healthcare provider right away.

Captopril is a medication that belongs to a class of drugs called ACE (angiotensin-converting enzyme) inhibitors. It works by blocking the action of a chemical in the body called angiotensin II, which causes blood vessels to narrow and release hormones that can increase blood pressure. By blocking the action of angiotensin II, captopril helps relax and widen blood vessels, which lowers blood pressure and improves blood flow.

Captopril is used to treat high blood pressure (hypertension), congestive heart failure, and to improve survival after a heart attack. It may also be used to protect the kidneys from damage due to diabetes or high blood pressure. The medication comes in the form of tablets that are taken by mouth, usually two to three times per day.

Common side effects of captopril include cough, dizziness, headache, and skin rash. More serious side effects may include allergic reactions, kidney problems, and changes in blood cell counts. It is important for patients taking captopril to follow their doctor's instructions carefully and report any unusual symptoms or side effects promptly.

Blood pressure is the force exerted by circulating blood on the walls of the blood vessels. It is measured in millimeters of mercury (mmHg) and is given as two figures:

1. Systolic pressure: This is the pressure when the heart pushes blood out into the arteries.
2. Diastolic pressure: This is the pressure when the heart rests between beats, allowing it to fill with blood.

Normal blood pressure for adults is typically around 120/80 mmHg, although this can vary slightly depending on age, sex, and other factors. High blood pressure (hypertension) is generally considered to be a reading of 130/80 mmHg or higher, while low blood pressure (hypotension) is usually defined as a reading below 90/60 mmHg. It's important to note that blood pressure can fluctuate throughout the day and may be affected by factors such as stress, physical activity, and medication use.

Tetrazoles are a class of heterocyclic aromatic organic compounds that contain a five-membered ring with four nitrogen atoms and one carbon atom. They have the chemical formula of C2H2N4. Tetrazoles are stable under normal conditions, but can decompose explosively when heated or subjected to strong shock.

In the context of medicinal chemistry, tetrazoles are sometimes used as bioisosteres for carboxylic acids, as they can mimic some of their chemical and biological properties. This has led to the development of several drugs that contain tetrazole rings, such as the antiviral drug tenofovir and the anti-inflammatory drug celecoxib.

However, it's important to note that 'tetrazoles' is not a medical term per se, but rather a chemical term that can be used in the context of medicinal chemistry or pharmacology.

A kidney, in medical terms, is one of two bean-shaped organs located in the lower back region of the body. They are essential for maintaining homeostasis within the body by performing several crucial functions such as:

1. Regulation of water and electrolyte balance: Kidneys help regulate the amount of water and various electrolytes like sodium, potassium, and calcium in the bloodstream to maintain a stable internal environment.

2. Excretion of waste products: They filter waste products from the blood, including urea (a byproduct of protein metabolism), creatinine (a breakdown product of muscle tissue), and other harmful substances that result from normal cellular functions or external sources like medications and toxins.

3. Endocrine function: Kidneys produce several hormones with important roles in the body, such as erythropoietin (stimulates red blood cell production), renin (regulates blood pressure), and calcitriol (activated form of vitamin D that helps regulate calcium homeostasis).

4. pH balance regulation: Kidneys maintain the proper acid-base balance in the body by excreting either hydrogen ions or bicarbonate ions, depending on whether the blood is too acidic or too alkaline.

5. Blood pressure control: The kidneys play a significant role in regulating blood pressure through the renin-angiotensin-aldosterone system (RAAS), which constricts blood vessels and promotes sodium and water retention to increase blood volume and, consequently, blood pressure.

Anatomically, each kidney is approximately 10-12 cm long, 5-7 cm wide, and 3 cm thick, with a weight of about 120-170 grams. They are surrounded by a protective layer of fat and connected to the urinary system through the renal pelvis, ureters, bladder, and urethra.

Antihypertensive agents are a class of medications used to treat high blood pressure (hypertension). They work by reducing the force and rate of heart contractions, dilating blood vessels, or altering neurohormonal activation to lower blood pressure. Examples include diuretics, beta blockers, ACE inhibitors, ARBs, calcium channel blockers, and direct vasodilators. These medications may be used alone or in combination to achieve optimal blood pressure control.

Hypertension is a medical term used to describe abnormally high blood pressure in the arteries, often defined as consistently having systolic blood pressure (the top number in a blood pressure reading) over 130 mmHg and/or diastolic blood pressure (the bottom number) over 80 mmHg. It is also commonly referred to as high blood pressure.

Hypertension can be classified into two types: primary or essential hypertension, which has no identifiable cause and accounts for about 95% of cases, and secondary hypertension, which is caused by underlying medical conditions such as kidney disease, hormonal disorders, or use of certain medications.

If left untreated, hypertension can lead to serious health complications such as heart attack, stroke, heart failure, and chronic kidney disease. Therefore, it is important for individuals with hypertension to manage their condition through lifestyle modifications (such as healthy diet, regular exercise, stress management) and medication if necessary, under the guidance of a healthcare professional.

Diabetic nephropathy is a kidney disease that occurs as a complication of diabetes. It is also known as diabetic kidney disease (DKD). This condition affects the ability of the kidneys to filter waste and excess fluids from the blood, leading to their accumulation in the body.

Diabetic nephropathy is caused by damage to the small blood vessels in the kidneys, which can occur over time due to high levels of glucose in the blood. This damage can lead to scarring and thickening of the kidney's filtering membranes, reducing their ability to function properly.

Symptoms of diabetic nephropathy may include proteinuria (the presence of protein in the urine), edema (swelling in the legs, ankles, or feet due to fluid retention), and hypertension (high blood pressure). Over time, if left untreated, diabetic nephropathy can progress to end-stage kidney disease, which requires dialysis or a kidney transplant.

Preventing or delaying the onset of diabetic nephropathy involves maintaining good control of blood sugar levels, keeping blood pressure under control, and making lifestyle changes such as quitting smoking, eating a healthy diet, and getting regular exercise. Regular monitoring of kidney function through urine tests and blood tests is also important for early detection and treatment of this condition.

I am not aware of a specific medical definition for "1-Sarcosine-8-Isoleucine Angiotensin II." It is possible that this term is being used to describe an altered or modified form of the peptide hormone angiotensin II.

Angiotensin II is a powerful vasoconstrictor and plays a central role in the regulation of blood pressure and fluid balance. Its octapeptide structure consists of eight amino acids, with the sequence Asp-Arg-Val-Tyr-Ile-His-Pro-Phe.

Modifying this sequence by replacing one or more amino acids can result in altered biological activity. In this case, "1-Sarcosine-8-Isoleucine" suggests that the first amino acid (Aspartic Acid) has been replaced with Sarcosine (N-methylglycine), and the eighth amino acid (Phenylalanine) has been replaced with Isoleucine.

However, without further context or research, it is difficult to provide a precise medical definition for this term. If you are seeking information on a specific scientific study or application, please provide more details so that I can give a more informed response.

Albuminuria is a medical condition that refers to the presence of albumin in the urine. Albumin is a type of protein normally found in the blood, but not in the urine. When the kidneys are functioning properly, they prevent large proteins like albumin from passing through into the urine. However, when the kidneys are damaged or not working correctly, such as in nephrotic syndrome or other kidney diseases, small amounts of albumin can leak into the urine.

The amount of albumin in the urine is often measured in milligrams per liter (mg/L) or in a spot urine sample, as the albumin-to-creatinine ratio (ACR). A small amount of albumin in the urine is called microalbuminuria, while a larger amount is called macroalbuminuria or proteinuria. The presence of albuminuria can indicate kidney damage and may be a sign of underlying medical conditions such as diabetes or high blood pressure. It is important to monitor and manage albuminuria to prevent further kidney damage and potential complications.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

Lisinopril is an angiotensin-converting enzyme (ACE) inhibitor, which is a type of medication used to treat various cardiovascular conditions. It works by blocking the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in relaxation and widening of blood vessels, decreased blood pressure, and increased blood flow.

Lisinopril is primarily used to treat hypertension (high blood pressure), congestive heart failure, and to improve survival after a heart attack. It may also be used to protect the kidneys from damage due to diabetes or high blood pressure. Additionally, it has been shown to reduce proteinuria (excess protein in urine) in patients with diabetic nephropathy.

Common side effects of Lisinopril include dizziness, headache, fatigue, and cough. More serious side effects may include angioedema (rapid swelling of the face, lips, tongue, or throat), hyperkalemia (elevated potassium levels), and impaired kidney function.

It is important to follow the prescribing physician's instructions carefully when taking Lisinopril and to report any unusual symptoms promptly. Regular monitoring of blood pressure, kidney function, and electrolyte levels may be necessary during treatment with this medication.

Aldosterone is a hormone produced by the adrenal gland. It plays a key role in regulating sodium and potassium balance and maintaining blood pressure through its effects on the kidneys. Aldosterone promotes the reabsorption of sodium ions and the excretion of potassium ions in the distal tubules and collecting ducts of the nephrons in the kidneys. This increases the osmotic pressure in the blood, which in turn leads to water retention and an increase in blood volume and blood pressure.

Aldosterone is released from the adrenal gland in response to a variety of stimuli, including angiotensin II (a peptide hormone produced as part of the renin-angiotensin-aldosterone system), potassium ions, and adrenocorticotropic hormone (ACTH) from the pituitary gland. The production of aldosterone is regulated by a negative feedback mechanism involving sodium levels in the blood. High sodium levels inhibit the release of aldosterone, while low sodium levels stimulate its release.

In addition to its role in maintaining fluid and electrolyte balance and blood pressure, aldosterone has been implicated in various pathological conditions, including hypertension, heart failure, and primary hyperaldosteronism (a condition characterized by excessive production of aldosterone).

Biphenyl compounds, also known as diphenyls, are a class of organic compounds consisting of two benzene rings linked by a single carbon-carbon bond. The chemical structure of biphenyl compounds can be represented as C6H5-C6H5. These compounds are widely used in the industrial sector, including as intermediates in the synthesis of other chemicals, as solvents, and in the production of plastics and dyes. Some biphenyl compounds also have biological activity and can be found in natural products. For example, some plant-derived compounds that belong to this class have been shown to have anti-inflammatory, antioxidant, and anticancer properties.

Angiotensin III is a hormone that is involved in the regulation of blood pressure and fluid balance in the body. It is formed by the enzymatic breakdown of angiotensin II, another hormone in the renin-angiotensin system (RAS). Angiotensin III has similar physiological effects as angiotensin II, including vasoconstriction (narrowing of blood vessels), stimulation of aldosterone release from the adrenal glands (which leads to sodium and water retention), and stimulation of thirst.

Angiotensin III is a peptide consisting of three amino acids, namely arginine-valine-tyrosine (Arg-Val-Tyr). It binds to and activates the angiotensin II receptor type 1 (AT1) and type 2 (AT2), which are found in various tissues throughout the body. The activation of these receptors leads to a range of physiological responses, including increased blood pressure, heart rate, and fluid volume.

Angiotensin III is less potent than angiotensin II in its ability to cause vasoconstriction and aldosterone release, but it has been shown to have important roles in the regulation of cardiovascular function, particularly during conditions of reduced renal perfusion or low blood pressure. It may also contribute to the development of certain diseases, such as hypertension, heart failure, and kidney disease.

Fumarates are the salts or esters of fumaric acid, a naturally occurring organic compound with the formula HO2C-CH=CH-CO2H. In the context of medical therapy, fumarates are used as medications for the treatment of psoriasis and multiple sclerosis.

One such medication is dimethyl fumarate (DMF), which is a stable salt of fumaric acid. DMF has anti-inflammatory and immunomodulatory properties, and it's used to treat relapsing forms of multiple sclerosis (MS) and moderate-to-severe plaque psoriasis.

The exact mechanism of action of fumarates in these conditions is not fully understood, but they are thought to modulate the immune system and have antioxidant effects. Common side effects of fumarate therapy include gastrointestinal symptoms such as diarrhea, nausea, and abdominal pain, as well as flushing and skin reactions.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Imidazoles are a class of heterocyclic organic compounds that contain a double-bonded nitrogen atom and two additional nitrogen atoms in the ring. They have the chemical formula C3H4N2. In a medical context, imidazoles are commonly used as antifungal agents. Some examples of imidazole-derived antifungals include clotrimazole, miconazole, and ketoconazole. These medications work by inhibiting the synthesis of ergosterol, a key component of fungal cell membranes, leading to increased permeability and death of the fungal cells. Imidazoles may also have anti-inflammatory, antibacterial, and anticancer properties.

Benzimidazoles are a class of heterocyclic compounds containing a benzene fused to a imidazole ring. They have a wide range of pharmacological activities and are used in the treatment of various diseases. Some of the benzimidazoles are used as antiparasitics, such as albendazole and mebendazole, which are effective against a variety of worm infestations. Other benzimidazoles have antifungal properties, such as thiabendazole and fuberidazole, and are used to treat fungal infections. Additionally, some benzimidazoles have been found to have anti-cancer properties and are being investigated for their potential use in cancer therapy.

Angiotensin II Type 2 Receptor Blockers (AT2RBs) are a class of drugs that selectively block the activation of Angiotensin II Type 2 receptors (AT2R). These receptors are found in various tissues throughout the body and play a role in regulating blood pressure, inflammation, and cell growth.

Angiotensin II is a hormone that constricts blood vessels and increases blood pressure. It binds to both AT1R and AT2R, but its effects are mainly mediated through AT1R. AT2RBs work by blocking the action of Angiotensin II at the AT2R, which can help lower blood pressure and reduce inflammation.

AT2RBs have been shown to have potential benefits in various clinical settings, including heart failure, diabetes, and kidney disease. However, their use is not as widespread as angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), which primarily target the AT1R.

Some examples of AT2RBs include EMA401, PD123319, and TRV120027.

Ramipril is an angiotensin-converting enzyme (ACE) inhibitor, which is a type of medication used to treat various cardiovascular conditions. It works by blocking the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, thereby causing relaxation and widening of blood vessels, decreasing blood pressure, and increasing blood flow.

Ramipril is primarily used for the treatment of hypertension (high blood pressure), heart failure, and the prevention of major cardiovascular events such as myocardial infarction (heart attack) and stroke in high-risk patients. It may also be used to improve survival after a heart attack.

The medication is available in oral tablet form and is typically taken once or twice daily, depending on the prescribed dosage. Side effects of ramipril can include cough, dizziness, headache, fatigue, nausea, and taste changes. Serious side effects are rare but may include kidney problems, hyperkalemia (high potassium levels), and angioedema (swelling of the face, lips, tongue, or throat).

It is important to follow the prescribing physician's instructions carefully when taking ramipril and to report any unusual symptoms or side effects promptly. Regular monitoring of blood pressure, kidney function, and potassium levels may be necessary during treatment with this medication.

Renal circulation refers to the blood flow specifically dedicated to the kidneys. The main function of the kidneys is to filter waste and excess fluids from the blood, which then get excreted as urine. To perform this function efficiently, the kidneys receive a substantial amount of the body's total blood supply - about 20-25% in a resting state.

The renal circulation process begins when deoxygenated blood from the rest of the body returns to the right side of the heart and is pumped into the lungs for oxygenation. Oxygen-rich blood then leaves the left side of the heart through the aorta, the largest artery in the body.

A portion of this oxygen-rich blood moves into the renal arteries, which branch directly from the aorta and supply each kidney with blood. Within the kidneys, these arteries divide further into smaller vessels called afferent arterioles, which feed into a network of tiny capillaries called the glomerulus within each nephron (the functional unit of the kidney).

The filtration process occurs in the glomeruli, where waste materials and excess fluids are separated from the blood. The resulting filtrate then moves through another set of capillaries, the peritubular capillaries, which surround the renal tubules (the part of the nephron that reabsorbs necessary substances back into the bloodstream).

The now-deoxygenated blood from the kidneys' capillary network coalesces into venules and then merges into the renal veins, which ultimately drain into the inferior vena cava and return the blood to the right side of the heart. This highly specialized circulation system allows the kidneys to efficiently filter waste while maintaining appropriate blood volume and composition.

A peptide fragment is a short chain of amino acids that is derived from a larger peptide or protein through various biological or chemical processes. These fragments can result from the natural breakdown of proteins in the body during regular physiological processes, such as digestion, or they can be produced experimentally in a laboratory setting for research or therapeutic purposes.

Peptide fragments are often used in research to map the structure and function of larger peptides and proteins, as well as to study their interactions with other molecules. In some cases, peptide fragments may also have biological activity of their own and can be developed into drugs or diagnostic tools. For example, certain peptide fragments derived from hormones or neurotransmitters may bind to receptors in the body and mimic or block the effects of the full-length molecule.

Messenger RNA (mRNA) is a type of RNA (ribonucleic acid) that carries genetic information copied from DNA in the form of a series of three-base code "words," each of which specifies a particular amino acid. This information is used by the cell's machinery to construct proteins, a process known as translation. After being transcribed from DNA, mRNA travels out of the nucleus to the ribosomes in the cytoplasm where protein synthesis occurs. Once the protein has been synthesized, the mRNA may be degraded and recycled. Post-transcriptional modifications can also occur to mRNA, such as alternative splicing and addition of a 5' cap and a poly(A) tail, which can affect its stability, localization, and translation efficiency.

Saralasin is a synthetic analog of the natural hormone angiotensin II, which is used in research and medicine. It acts as an antagonist of the angiotensin II receptor, blocking its effects. Saralasin is primarily used in research to study the role of the renin-angiotensin system in various physiological processes. In clinical medicine, it has been used in the diagnosis and treatment of conditions such as hypertension and pheochromocytoma, although its use is not widespread due to the availability of more effective and selective drugs.

Hemodynamics is the study of how blood flows through the cardiovascular system, including the heart and the vascular network. It examines various factors that affect blood flow, such as blood volume, viscosity, vessel length and diameter, and pressure differences between different parts of the circulatory system. Hemodynamics also considers the impact of various physiological and pathological conditions on these variables, and how they in turn influence the function of vital organs and systems in the body. It is a critical area of study in fields such as cardiology, anesthesiology, and critical care medicine.

"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.

Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.

It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.

Vasoconstrictor agents are substances that cause the narrowing of blood vessels by constricting the smooth muscle in their walls. This leads to an increase in blood pressure and a decrease in blood flow. They work by activating the sympathetic nervous system, which triggers the release of neurotransmitters such as norepinephrine and epinephrine that bind to alpha-adrenergic receptors on the smooth muscle cells of the blood vessel walls, causing them to contract.

Vasoconstrictor agents are used medically for a variety of purposes, including:

* Treating hypotension (low blood pressure)
* Controlling bleeding during surgery or childbirth
* Relieving symptoms of nasal congestion in conditions such as the common cold or allergies

Examples of vasoconstrictor agents include phenylephrine, oxymetazoline, and epinephrine. It's important to note that prolonged use or excessive doses of vasoconstrictor agents can lead to rebound congestion and other adverse effects, so they should be used with caution and under the guidance of a healthcare professional.

The endothelium is a thin layer of simple squamous epithelial cells that lines the interior surface of blood vessels, lymphatic vessels, and heart chambers. The vascular endothelium, specifically, refers to the endothelial cells that line the blood vessels. These cells play a crucial role in maintaining vascular homeostasis by regulating vasomotor tone, coagulation, platelet activation, inflammation, and permeability of the vessel wall. They also contribute to the growth and repair of the vascular system and are involved in various pathological processes such as atherosclerosis, hypertension, and diabetes.

Renal hypertension, also known as renovascular hypertension, is a type of secondary hypertension (high blood pressure) that is caused by narrowing or obstruction of the renal arteries or veins, which supply blood to the kidneys. This can lead to decreased blood flow and oxygen delivery to the kidney tissue, activating the renin-angiotensin-aldosterone system (RAAS) and resulting in increased peripheral vascular resistance, sodium retention, and extracellular fluid volume, ultimately causing hypertension.

Renal hypertension can be classified into two types:

1. Renin-dependent renal hypertension: This is caused by a decrease in blood flow to the kidneys, leading to increased renin release from the juxtaglomerular cells of the kidney. Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor that causes an increase in peripheral vascular resistance and blood pressure.
2. Renin-independent renal hypertension: This is caused by increased sodium retention and extracellular fluid volume, leading to an increase in blood pressure. This can be due to various factors such as obstructive sleep apnea, primary aldosteronism, or pheochromocytoma.

Renal hypertension is often asymptomatic but can lead to serious complications such as kidney damage, heart failure, and stroke if left untreated. Diagnosis of renal hypertension involves imaging studies such as renal artery duplex ultrasound, CT angiography, or magnetic resonance angiography (MRA) to identify any narrowing or obstruction in the renal arteries or veins. Treatment options include medications such as ACE inhibitors, angiotensin receptor blockers (ARBs), calcium channel blockers, and diuretics, as well as interventions such as angioplasty and stenting to improve blood flow to the kidneys.

A sodium-restricted diet is a meal plan designed to limit the amount of sodium (salt) intake. The recommended daily sodium intake for adults is less than 2,300 milligrams (mg), but for those with certain medical conditions such as high blood pressure, heart failure, or chronic kidney disease, a lower daily sodium limit of 1,500 to 2,000 mg may be recommended.

A sodium-restricted diet typically involves avoiding processed and packaged foods, which are often high in sodium, and limiting the use of salt when cooking or at the table. Fresh fruits, vegetables, lean proteins, and whole grains are encouraged as they are naturally low in sodium. It is important to read food labels carefully, as some foods may contain hidden sources of sodium.

Adhering to a sodium-restricted diet can help manage blood pressure, reduce fluid retention, and decrease the risk of heart disease and stroke. However, it is important to consult with a healthcare provider or a registered dietitian before starting any new diet plan to ensure that it meets individual nutritional needs and medical conditions.

Teprotide is not a medical condition but rather a medication. It's a synthetic peptide that acts as an inhibitor of the enzyme angiotensin-converting enzyme (ACE). ACE plays a crucial role in regulating blood pressure and fluid balance by converting angiotensin I to angiotensin II, which is a potent vasoconstrictor. By blocking this conversion, teprotide can help lower blood pressure and reduce the workload on the heart.

Teprotide was initially used in clinical trials for the treatment of hypertension and heart failure but has since been largely replaced by other ACE inhibitors with more favorable pharmacokinetic properties. It is still occasionally used in research settings to study the renin-angiotensin system's role in various physiological processes.

Angiotensin amide is not a medical term itself, but it refers to a form of angiotensin II, which is a potent vasoconstrictor (a substance that narrows blood vessels) in the body. Angiotensin II is formed from angiotensin I through the action of an enzyme called angiotensin-converting enzyme (ACE).

Angiotensin II amide, also known as angiotensin II-amide or angiotensin II-(1-8), refers to the biologically active form of angiotensin II. It is an octapeptide with the amino acid sequence Asp-Arg-Val-Tyr-Ile-His-Pro-Phe, and its carboxy terminus is amidated (has an amide group instead of a free carboxyl group). This amide form of angiotensin II is more stable than the non-amidated form and has a longer half-life in circulation.

Angiotensin II amide plays a crucial role in regulating blood pressure and fluid balance by causing vasoconstriction, stimulating aldosterone release from the adrenal glands (which leads to sodium and water retention), and promoting thirst. Drugs that inhibit ACE or block angiotensin II receptors are commonly used in the treatment of hypertension and heart failure.

SHR (Spontaneously Hypertensive Rats) are an inbred strain of rats that were originally developed through selective breeding for high blood pressure. They are widely used as a model to study hypertension and related cardiovascular diseases, as well as neurological disorders such as stroke and dementia.

Inbred strains of animals are created by mating genetically identical individuals (siblings or offspring) for many generations, resulting in a population that is highly homozygous at all genetic loci. This means that the animals within an inbred strain are essentially genetically identical to one another, which makes them useful for studying the effects of specific genes or environmental factors on disease processes.

SHR rats develop high blood pressure spontaneously, without any experimental manipulation, and show many features of human hypertension, such as increased vascular resistance, left ventricular hypertrophy, and renal dysfunction. They also exhibit a number of behavioral abnormalities, including hyperactivity, impulsivity, and cognitive deficits, which make them useful for studying the neurological consequences of hypertension and other cardiovascular diseases.

Overall, inbred SHR rats are an important tool in biomedical research, providing a valuable model for understanding the genetic and environmental factors that contribute to hypertension and related disorders.

Enalaprilat is a medication that belongs to a class of drugs called ACE (angiotensin-converting enzyme) inhibitors. It is the active metabolite of Enalapril. Enalaprilat works by blocking the action of angiotensin-converting enzyme, which helps to relax and widen blood vessels, thereby reducing blood pressure and increasing blood flow.

Enalaprilat is primarily used to treat hypertension (high blood pressure), heart failure, and to improve survival after a heart attack. It is administered intravenously in a hospital setting, and its effects are usually seen within 15 minutes of administration. Common side effects of Enalaprilat include hypotension (low blood pressure), dizziness, headache, and nausea.

Renovascular hypertension is a type of secondary hypertension (high blood pressure) that is caused by renal artery stenosis or narrowing. This condition reduces blood flow to the kidneys, leading to the activation of the renin-angiotensin-aldosterone system (RAAS), which causes an increase in peripheral vascular resistance and blood volume, resulting in hypertension.

Renovascular hypertension is often seen in people with atherosclerosis or fibromuscular dysplasia, which are the most common causes of renal artery stenosis. Other conditions that can lead to renovascular hypertension include vasculitis, blood clots, and compression of the renal artery by nearby structures.

Diagnosis of renovascular hypertension typically involves imaging studies such as duplex ultrasound, CT angiography, or magnetic resonance angiography to visualize the renal arteries and assess for stenosis. Treatment may involve medications to control blood pressure, lifestyle modifications, and procedures such as angioplasty and stenting to open up the narrowed renal artery. In some cases, surgery may be necessary to restore blood flow to the kidney.

I'm sorry for any confusion, but "Pyridines" is not a medical term. It is a chemical term that refers to a class of organic compounds with the chemical structure of a six-membered ring containing one nitrogen atom and five carbon atoms (heterocyclic aromatic compound).

In a biological or medical context, pyridine derivatives can be found in various natural and synthetic substances. For example, some medications contain pyridine rings as part of their chemical structure. However, "Pyridines" itself is not a medical term or condition.

WKY (Wistar Kyoto) is not a term that refers to "rats, inbred" in a medical definition. Instead, it is a strain of laboratory rat that is widely used in biomedical research. WKY rats are an inbred strain, which means they are the result of many generations of brother-sister matings, resulting in a genetically uniform population.

WKY rats originated from the Wistar Institute in Philadelphia and were established as a normotensive control strain to contrast with other rat strains that exhibit hypertension. They have since been used in various research areas, including cardiovascular, neurological, and behavioral studies. Compared to other commonly used rat strains like the spontaneously hypertensive rat (SHR), WKY rats are known for their lower blood pressure, reduced stress response, and greater emotionality.

In summary, "WKY" is a designation for an inbred strain of laboratory rat that is often used as a control group in biomedical research due to its normotensive characteristics.

Furosemide is a loop diuretic medication that is primarily used to treat edema (fluid retention) associated with various medical conditions such as heart failure, liver cirrhosis, and kidney disease. It works by inhibiting the sodium-potassium-chloride cotransporter in the ascending loop of Henle in the kidneys, thereby promoting the excretion of water, sodium, and chloride ions. This increased urine output helps reduce fluid accumulation in the body and lower blood pressure.

Furosemide is also known by its brand names Lasix and Frusid. It can be administered orally or intravenously, depending on the patient's condition and the desired rate of diuresis. Common side effects include dehydration, electrolyte imbalances, hearing loss (in high doses), and increased blood sugar levels.

It is essential to monitor kidney function, electrolyte levels, and fluid balance while using furosemide to minimize potential adverse effects and ensure appropriate treatment.

A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.

The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.

The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.

In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.

A smooth muscle within the vascular system refers to the involuntary, innervated muscle that is found in the walls of blood vessels. These muscles are responsible for controlling the diameter of the blood vessels, which in turn regulates blood flow and blood pressure. They are called "smooth" muscles because their individual muscle cells do not have the striations, or cross-striped patterns, that are observed in skeletal and cardiac muscle cells. Smooth muscle in the vascular system is controlled by the autonomic nervous system and by hormones, and can contract or relax slowly over a period of time.

Sodium is an essential mineral and electrolyte that is necessary for human health. In a medical context, sodium is often discussed in terms of its concentration in the blood, as measured by serum sodium levels. The normal range for serum sodium is typically between 135 and 145 milliequivalents per liter (mEq/L).

Sodium plays a number of important roles in the body, including:

* Regulating fluid balance: Sodium helps to regulate the amount of water in and around your cells, which is important for maintaining normal blood pressure and preventing dehydration.
* Facilitating nerve impulse transmission: Sodium is involved in the generation and transmission of electrical signals in the nervous system, which is necessary for proper muscle function and coordination.
* Assisting with muscle contraction: Sodium helps to regulate muscle contractions by interacting with other minerals such as calcium and potassium.

Low sodium levels (hyponatremia) can cause symptoms such as confusion, seizures, and coma, while high sodium levels (hypernatremia) can lead to symptoms such as weakness, muscle cramps, and seizures. Both conditions require medical treatment to correct.

Norepinephrine, also known as noradrenaline, is a neurotransmitter and a hormone that is primarily produced in the adrenal glands and is released into the bloodstream in response to stress or physical activity. It plays a crucial role in the "fight-or-flight" response by preparing the body for action through increasing heart rate, blood pressure, respiratory rate, and glucose availability.

As a neurotransmitter, norepinephrine is involved in regulating various functions of the nervous system, including attention, perception, motivation, and arousal. It also plays a role in modulating pain perception and responding to stressful or emotional situations.

In medical settings, norepinephrine is used as a vasopressor medication to treat hypotension (low blood pressure) that can occur during septic shock, anesthesia, or other critical illnesses. It works by constricting blood vessels and increasing heart rate, which helps to improve blood pressure and perfusion of vital organs.

Valine is an essential amino acid, meaning it cannot be produced by the human body and must be obtained through diet. It is a hydrophobic amino acid, with a branched side chain, and is necessary for the growth, repair, and maintenance of tissues in the body. Valine is also important for muscle metabolism, and is often used by athletes as a supplement to enhance physical performance. Like other essential amino acids, valine must be obtained through foods such as meat, fish, dairy products, and legumes.

Vasoconstriction is a medical term that refers to the narrowing of blood vessels due to the contraction of the smooth muscle in their walls. This process decreases the diameter of the lumen (the inner space of the blood vessel) and reduces blood flow through the affected vessels. Vasoconstriction can occur throughout the body, but it is most noticeable in the arterioles and precapillary sphincters, which control the amount of blood that flows into the capillary network.

The autonomic nervous system, specifically the sympathetic division, plays a significant role in regulating vasoconstriction through the release of neurotransmitters like norepinephrine (noradrenaline). Various hormones and chemical mediators, such as angiotensin II, endothelin-1, and serotonin, can also induce vasoconstriction.

Vasoconstriction is a vital physiological response that helps maintain blood pressure and regulate blood flow distribution in the body. However, excessive or prolonged vasoconstriction may contribute to several pathological conditions, including hypertension, stroke, and peripheral vascular diseases.

Nephrectomy is a surgical procedure in which all or part of a kidney is removed. It may be performed due to various reasons such as severe kidney damage, kidney cancer, or living donor transplantation. The type of nephrectomy depends on the reason for the surgery - a simple nephrectomy involves removing only the affected portion of the kidney, while a radical nephrectomy includes removal of the whole kidney along with its surrounding tissues like the adrenal gland and lymph nodes.

Bradykinin is a naturally occurring peptide in the human body, consisting of nine amino acids. It is a potent vasodilator and increases the permeability of blood vessels, causing a local inflammatory response. Bradykinin is formed from the breakdown of certain proteins, such as kininogen, by enzymes called kininases or proteases, including kallikrein. It plays a role in several physiological processes, including pain transmission, blood pressure regulation, and the immune response. In some pathological conditions, such as hereditary angioedema, bradykinin levels can increase excessively, leading to symptoms like swelling, redness, and pain.

Chymases are a type of enzyme that belong to the family of serine proteases. They are found in various tissues and organs, including the heart, lungs, and immune cells called mast cells. Chymases play a role in several physiological and pathological processes, such as inflammation, tissue remodeling, and blood pressure regulation.

One of the most well-known chymases is found in the mast cells and is often referred to as "mast cell chymase." This enzyme can cleave and activate various proteins, including angiotensin I to angiotensin II, a potent vasoconstrictor that increases blood pressure. Chymases have also been implicated in the development of cardiovascular diseases, such as hypertension and heart failure, as well as respiratory diseases like asthma and chronic obstructive pulmonary disease (COPD).

In summary, chymases are a group of serine protease enzymes that play important roles in various physiological and pathological processes, particularly in inflammation, tissue remodeling, and blood pressure regulation.

The adrenal glands are a pair of endocrine glands that are located on top of the kidneys. Each gland has two parts: the outer cortex and the inner medulla. The adrenal cortex produces hormones such as cortisol, aldosterone, and androgens, which regulate metabolism, blood pressure, and other vital functions. The adrenal medulla produces catecholamines, including epinephrine (adrenaline) and norepinephrine (noradrenaline), which help the body respond to stress by increasing heart rate, blood pressure, and alertness.

The myocardium is the middle layer of the heart wall, composed of specialized cardiac muscle cells that are responsible for pumping blood throughout the body. It forms the thickest part of the heart wall and is divided into two sections: the left ventricle, which pumps oxygenated blood to the rest of the body, and the right ventricle, which pumps deoxygenated blood to the lungs.

The myocardium contains several types of cells, including cardiac muscle fibers, connective tissue, nerves, and blood vessels. The muscle fibers are arranged in a highly organized pattern that allows them to contract in a coordinated manner, generating the force necessary to pump blood through the heart and circulatory system.

Damage to the myocardium can occur due to various factors such as ischemia (reduced blood flow), infection, inflammation, or genetic disorders. This damage can lead to several cardiac conditions, including heart failure, arrhythmias, and cardiomyopathy.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

Heart rate is the number of heartbeats per unit of time, often expressed as beats per minute (bpm). It can vary significantly depending on factors such as age, physical fitness, emotions, and overall health status. A resting heart rate between 60-100 bpm is generally considered normal for adults, but athletes and individuals with high levels of physical fitness may have a resting heart rate below 60 bpm due to their enhanced cardiovascular efficiency. Monitoring heart rate can provide valuable insights into an individual's health status, exercise intensity, and response to various treatments or interventions.

Cardiomegaly is a medical term that refers to an enlarged heart. It can be caused by various conditions such as high blood pressure, heart valve problems, cardiomyopathy, or fluid accumulation around the heart (pericardial effusion). Cardiomegaly can be detected through imaging tests like chest X-rays or echocardiograms. Depending on the underlying cause, treatment options may include medications, lifestyle changes, or in some cases, surgery. It is important to consult with a healthcare professional for proper diagnosis and treatment.

The aorta is the largest artery in the human body, which originates from the left ventricle of the heart and carries oxygenated blood to the rest of the body. It can be divided into several parts, including the ascending aorta, aortic arch, and descending aorta. The ascending aorta gives rise to the coronary arteries that supply blood to the heart muscle. The aortic arch gives rise to the brachiocephalic, left common carotid, and left subclavian arteries, which supply blood to the head, neck, and upper extremities. The descending aorta travels through the thorax and abdomen, giving rise to various intercostal, visceral, and renal arteries that supply blood to the chest wall, organs, and kidneys.

An amide is a functional group or a compound that contains a carbonyl group (a double-bonded carbon atom) and a nitrogen atom. The nitrogen atom is connected to the carbonyl carbon atom by a single bond, and it also has a lone pair of electrons. Amides are commonly found in proteins and peptides, where they form amide bonds (also known as peptide bonds) between individual amino acids.

The general structure of an amide is R-CO-NHR', where R and R' can be alkyl or aryl groups. Amides can be classified into several types based on the nature of R and R' substituents:

* Primary amides: R-CO-NH2
* Secondary amides: R-CO-NHR'
* Tertiary amides: R-CO-NR''R'''

Amides have several important chemical properties. They are generally stable and resistant to hydrolysis under neutral or basic conditions, but they can be hydrolyzed under acidic conditions or with strong bases. Amides also exhibit a characteristic infrared absorption band around 1650 cm-1 due to the carbonyl stretching vibration.

In addition to their prevalence in proteins and peptides, amides are also found in many natural and synthetic compounds, including pharmaceuticals, dyes, and polymers. They have a wide range of applications in chemistry, biology, and materials science.

Hydralazine is an antihypertensive medication, which means it is used to treat high blood pressure. It works by relaxing and widening the blood vessels, making it easier for the heart to pump blood through the body. This can help reduce the workload on the heart and lower blood pressure. Hydralazine is available in oral tablet form and is typically prescribed to be taken several times a day.

Hydralazine belongs to a class of medications called vasodilators, which work by relaxing the muscle in the walls of the blood vessels, causing them to widen. This increases the amount of blood that can flow through the blood vessels and reduces the pressure within them. Hydralazine is often used in combination with other medications to treat high blood pressure.

It's important to note that hydralazine should be used under the close supervision of a healthcare provider, as it can cause side effects such as headache, dizziness, and rapid heartbeat. It may also interact with certain other medications, so it is important to inform your doctor of all medications you are taking before starting hydralazine.

Natriuresis is the process or condition of excreting an excessive amount of sodium (salt) through urine. It is a physiological response to high sodium levels in the body, which can be caused by various factors such as certain medical conditions (e.g., kidney disease, heart failure), medications, or dietary habits. The increased excretion of sodium helps regulate the body's water balance and maintain normal blood pressure. However, persistent natriuresis may indicate underlying health issues that require medical attention.

The renin-angiotensin system (RAS), or renin-angiotensin-aldosterone system (RAAS), is a hormone system that regulates blood ... In the fetus, the renin-angiotensin system is predominantly a sodium-losing system,[citation needed] as angiotensin II has ... Angiotensin II is the major bioactive product of the renin-angiotensin system, binding to receptors on intraglomerular ... Nakagawa P, Gomez J, Grobe JL, Sigmund CD (January 2020). "The Renin-Angiotensin System in the Central Nervous System and Its ...
... the natriuretic peptides and the kallikrein-kinin system. Journal of the Renin-Angiotensin-Aldosterone System is abstracted and ... Journal of the Renin-Angiotensin-Aldosterone System is a peer-reviewed academic journal that publishes papers in the field of ... Journal of the Renin-Angiotensin-Aldosterone System is a resource for biomedical professionals, including basic scientists and ... Journal of the Renin-Angiotensin-Aldosterone System also publishes research on other peptides, such as vasopressin, ...
The production of aldosterone is regulated via the renin-angiotensin II-aldosterone system, a system composed of baroreceptors ... Fountain JH, Kaur J, Lappin SL (2023). "Physiology, Renin Angiotensin System". StatPearls. Treasure Island (FL): StatPearls ... As the hormones produced are regulated by a range of systems in the body, overactivity of the adrenal glands can be caused by ... Changes in the homeostasis of the human body, such as osmolality are detected by the system, which causes a chain reaction that ...
Renin-angiotensin system (RAS): This system is generally known for its long-term adjustment of arterial pressure. This system ... Renin converts angiotensinogen to angiotensin I, which is converted by angiotensin converting enzyme to angiotensin II. ... Renin converts angiotensinogen (inactive form) to angiotensin I (active form). Angiotensin I flows in the bloodstream until it ... Fountain J, Lappin SL (January 2022). "Physiology, Renin Angiotensin System.". StatPearls. Treasure Island, FL: StatPearls ...
The compression is believed to cause activation of the renin-angiotensin-aldosterone system (RAAS) via microvascular ischemia.[ ... Fountain, JH; Lappin, SL (July 27, 2020). Physiology, Renin Angiotensin System. Treasure Island, FL: StatPearls Publishing. ... blood pressure seen in Page kidney is thought to be caused by the activation of the renin-angiotensin-aldosterone system (RAAS ... Medical treatment involves use of an angiotensin-converting enzyme inhibitor (ACEi) or an angiotensin receptor blocker (ARB) to ...
Inhibitors of the renin-angiotensin system (RAS) are recommended in heart failure. The angiotensin receptor-neprilysin ... mediated by long-term activation of neurohormonal systems such as the renin-angiotensin system and the sympathoadrenal system, ... renin-angiotensin system inhibitors; and beta-blockers. In 2011, nonhypertensive heart failure was one of the 10 most expensive ... Vasopressin levels are usually increased, along with renin, angiotensin II, and catecholamines to compensate for reduced ...
Ruilope LM, Tamargo J (April 2017). "Renin-angiotensin system blockade: Finerenone". Nephrologie & Therapeutique. 13 Suppl 1: ...
... which stimulates the renin-angiotensin system, producing angiotensin I which is converted by Angio-Tensin Converting Enzyme ( ... Homeostasis Renin-angiotensin system "CV Physiology , Autoregulation of Organ Blood Flow". www.cvphysiology.com. Retrieved 2020 ... This is so-called "steady-state system". An example is a system in which a protein P that is a product of gene G "positively ... that system's response to stimuli. While most systems of the body show some degree of autoregulation, it is most clearly ...
Oakes JM, Fuchs RM, Gardner JD, Lazartigues E, Yue X (November 2018). "Nicotine and the renin-angiotensin system". American ... Many of the observed negative effects from e-cigarette use concerning the nervous system and the sensory system are possibly ... "Electronic Nicotine Delivery Systems and Electronic Non-Nicotine Delivery Systems (ENDS/ENNDS)" (PDF). World Health ... E-cigarettes could harm the respiratory system. Vaping induces irritation of the upper and lower respiratory system. The ...
This activates the renin-angiotensin system. Among other actions, it causes renal tubules (i.e. the distal convoluted tubules ... The activated renin-angiotensin system stimulates the zona glomerulosa of the adrenal cortex which in turn secretes the hormone ... might suggest a problem with either the kidney or cardiovascular system. If blood pressure is low (hypotension), the filtration ...
... (EC 3.4.15.1), or ACE, is a central component of the renin-angiotensin system (RAS), which ... ACE inhibitors Angiotensin-converting enzyme 2 (ACE2) Hypotensive transfusion reaction Renin-angiotensin system GRCh38: Ensembl ... Renin-Angiotensin Systems: State of the Art. 35 (6): 769-773. doi:10.1016/S1357-2725(02)00309-6. PMID 12676162. Zhang R, Xu X, ... ACE is a central component of the renin-angiotensin system (RAS), which controls blood pressure by regulating the volume of ...
... the renin-angiotensin-aldosterone system as a paradigm". Journal of the Renin-Angiotensin-Aldosterone System. 1 (4): 316-324. ... "Angiotensin II receptor blocker", Wikipedia, 2022-07-26, retrieved 2022-08-10 Wilson JX (1984). "The renin-angiotensin system ... Elements of the renin-angiotensin system have been widely studied in a large variety of vertebrate animals including amphibians ... Arima S, Ito S (November 2001). "New insights into actions of the renin-angiotensin system in the kidney: concentrating on the ...
Journal of the Renin-Angiotensin-Aldosterone System. 12 (3): 231-237. doi:10.1177/1470320310388440. PMID 21163863. S2CID ... The system is present in New Spain's first national census (in 1793), in which castizo, pardo, mulatto and zambo are also ... An extensive caste system assigned a name to each possible racial combination; unlike later definitions of mestizo, in these ... Although the caste system and racial classification were officially abandoned when Mexico became independent, the label mestizo ...
... the renin-angiotensin-aldosterone system as a paradigm". Journal of the Renin-Angiotensin-Aldosterone System. 1 (4): 316-24. ... is only expressed in the zona glomerulosa of the adrenal cortex and is primarily regulated by the renin-angiotensin system. It ... Martsev SP, Chashchin VL, Akhrem AA [in Belarusian] (February 1985). "[Reconstruction and study of a multi-enzyme system by 11 ... Brown RD, Strott CA, Liddle GW (June 1972). "Site of stimulation of aldosterone biosynthesis by angiotensin and potassium". The ...
Journal of the Renin-Angiotensin-Aldosterone System. 15 (1): 88-96. doi:10.1177/1470320313475910. PMID 23435582. Liu P, Jing Y ... Tomblin FA, Lucas KH (February 2001). "Lysine for management of herpes labialis". American Journal of Health-System Pharmacy. ... and also has functions in the immune system's reaction to infection. Arginine is also a precursor for urea, ornithine, and ... cholinergic system dysfunction, stress vulnerability and neurodevelopmental disruption, have been linked to the aetiology and/ ...
Segura J, Ruilope LM (October 2007). "Obesity, essential hypertension and renin-angiotensin system". Public Health Nutrition. ... This list includes also other factors like the aging, renin related patterns, or sympathetic nervous system related issues. II- ... Task force 3: Prevention and intervention research in primary care which covers all health systems, policy, and primary care ...
Wilson JX (1984). "The renin-angiotensin system in nonmammalian vertebrates". Endocrine Reviews. 5 (1): 45-61. doi:10.1210/edrv ... The human endocrine system consists of several systems that operate via feedback loops. Several important feedback systems are ... The endocrine system has three sets of endocrine outputs which include the magnocellular system, the parvocellular system, and ... All vertebrates have some form of a renin-angiotensin axis, and all tetrapods have aldosterone as a primary mineralocorticoid. ...
The activity of local renin-angiotensin systems and alternative pathways of angiotensin II formation may make an important ... is the renin-angiotensin-aldosterone system. Renin is a circulating enzyme that participates in maintaining extracellular ... Recent studies claim that obesity is a risk factor for hypertension because of activation of the renin-angiotensin system (RAS ... Saitoh S (April 2009). "[Insulin resistance and renin-angiotensin-aldosterone system]". Nippon Rinsho. Japanese Journal of ...
Mineralocorticoid secretion is regulated mainly by the renin-angiotensin-aldosterone system (RAAS), the concentration of ... Crowley, SD; Coffman, TM (2012). "Recent advances involving the renin-angiotensin system". Experimental Cell Research. 318 (9 ... which are under regulation of the renin-angiotensin system instead. Congenital adrenal hyperplasia is a family of congenital ... which starts a cascade of reactions that lead to formation of angiotensin II. Angiotensin receptors in cells of the zona ...
Journal of the Renin-Angiotensin-Aldosterone System. 9 (4): 221-5. doi:10.1177/1470320308096405. PMID 19126663. S2CID 206729914 ... Several different classification systems for the progestins exist, but the one most commonly used system recapitulates the ... The estrogen and progestogen in COCPs have other effects on the reproductive system, but these have not been shown to ... Rang HP, Dale MM, Ritter JM, Flower RJ, Henderson G (2012). "The reproductive system". Rang and Dale's pharmacology (7th ed.). ...
Journal of the Renin-Angiotensin-Aldosterone System. 11 (1): 57-66. doi:10.1177/1470320309347790. PMID 19880657. Liu C, Zhou Q ... Agents acting on the renin-angiotensin system, Experimental drugs, Imidazopyridines, All stub articles, Pharmacology stubs). ... and with lower affinity as an agonist of angiotensin II receptor type 2, mimicking the action of angiotensin II. Its practical ... applications to date have been limited to scientific research into the function of the angiotensin receptor system, but it has ...
Brasier AR, Recinos A, Eledrisi MS (August 2002). "Vascular inflammation and the renin-angiotensin system". Arteriosclerosis, ... as well as cells from other organ systems. Hence, targeting cytokines and their receptors is an effective means of treating ...
Drapala A, Sikora M, Ufnal M (September 2014). "Statins, the renin-angiotensin-aldosterone system and hypertension - a tale of ... Journal of the Renin-Angiotensin-Aldosterone System. 15 (3): 250-258. doi:10.1177/1470320314531058. PMID 25037529. Mondul AM, ... American Journal of Health-System Pharmacy. 74 (11): 786-793. doi:10.2146/ajhp160714. PMID 28546301. S2CID 3825396. Link E, ...
The renin-angiotensin system and its blockers. Igić R, Škrbić R. Srp Arh Celok Lek. 2014 Nov-Dec;142(11-12):756-63. doi: ... Igić R, Škrbić R. The renin-angiotensin system and its blockers. Srp Arh Celok Lek 2014;142:756-63. Sokolova-Djokic L, Zizic- ... His research career centered on the Renin-angiotensin system. While at the Universities of Tuzla and Banja Luka in the 1980s, ... Igić R. Four decades of ocular renin-angiotensin and kallikrein-kinin systems (1977-2017). Exp Eye Res 2018;166:74-83. doi: ...
Journal of the Renin-Angiotensin-Aldosterone System. 3 (1): 1-15. doi:10.3317/jraas.2002.001. PMID 11984741. S2CID 11382836. ... Endothelins are implicated in vascular diseases of several organ systems, including the heart, lungs, kidneys, and brain. As of ... Kedzierski RM, Yanagisawa M (2001). "Endothelin system: the double-edged sword in health and disease". Annual Review of ... Endothelin-1 is the most powerful endogenous chemical affecting vascular tone across organ systems. Secretion of endothelin-1 ...
Journal of the Renin-Angiotensin-Aldosterone System. 12 (3): 231-237. doi:10.1177/1470320310388440. PMID 21163863. S2CID ... Nonetheless, the system was not completely rigid and elements such as social class, social relations and who a person descended ... However, due to the abolition of the caste system, the division became more about money and social class and less about ... "Renin gene haplotype diversity and linkage disequilibrium in two Mexican and one German population samples". ...
Journal of the Renin-Angiotensin-Aldosterone System. 12 (3): 231-237. doi:10.1177/1470320310388440. PMID 21163863. S2CID ... intermarriage and mixed race offspring created an elaborate caste system. This system broke down in the very late Spanish ... The system of interconnected lakes, of which Texcoco formed the center, had the form of a rabbit, which the Mesoamericans ... Even though it still arranges persons along the line between indigenous and European, in practice the classificatory system is ...
Karlberg BE (April 1993). "Cough and inhibition of the renin-angiotensin system". Journal of Hypertension Supplement. 11 (3): ... The kinin-kallikrein system makes bradykinin by proteolytic cleavage of its kininogen precursor, high-molecular-weight ... On the basis of this finding, a non-protein analog of BPF which was effective orally was developed: the first angiotensin ... Bradykinin is also thought to be the cause of the dry cough in some patients on widely prescribed angiotensin-converting enzyme ...
Peptides of the renin-angiotensin system: angiotensin II and angiotensin (1-7) Fibroblast growth factor 2 Parathyroid hormone- ... Kumar R, Singh VP, Baker KM (July 2007). "The intracellular renin-angiotensin system: a new paradigm". Trends in Endocrinology ... PMID 16615083.Singh VP, Baker KM, Kumar R (Apr 2008). "Activation of the intracellular renin-angiotensin system in cardiac ... The paracrine system is one where nearby cells get hormones from a cell, and change the functioning of those nearby cells. The ...
Renin-Angiotensin System and Endothelial Dysfunction". Cells. 9 (7): 1652. doi:10.3390/cells9071652. PMC 7407648. PMID 32660065 ...
The renin-angiotensin system (RAS), or renin-angiotensin-aldosterone system (RAAS), is a hormone system that regulates blood ... In the fetus, the renin-angiotensin system is predominantly a sodium-losing system,[citation needed] as angiotensin II has ... Angiotensin II is the major bioactive product of the renin-angiotensin system, binding to receptors on intraglomerular ... Nakagawa P, Gomez J, Grobe JL, Sigmund CD (January 2020). "The Renin-Angiotensin System in the Central Nervous System and Its ...
SARS-CoV-2 gains cell entry via angiotensin-converting enzyme (ACE) 2, a membrane-bound enzyme of the ... Antlanger, M. et al. Molecular remodeling of the renin-angiotensin system after kidney transplantation. J. Renin. Angiotensin ... renin-angiotensin system (RAS). ACE2 counteracts angiotensin II by converting it to potentially protective angiotensin 1-7. ... Ratio of angiotensin II to angiotensin I (A, B) The ratio of angiotensin II to angiotensin I (ALT-S) was reduced in severe ...
Fetal renin-angiotensin system edit In the fetus, the renin-angiotensin system is predominantly a sodium-losing system,[ ... The renin-angiotensin system (RAS), or renin-angiotensin-aldosterone system (RAAS), is a hormone system that regulates blood ... Local renin-angiotensin systems edit Locally expressed renin-angiotensin systems have been found in a number of tissues, ... Angiotensin II is the major bioactive product of the renin-angiotensin system, binding to receptors on intraglomerular ...
... J Am Soc ... We compared the effects of two renin-angiotensin-aldosterone system (RAAS) inhibitors (quinapril and aliskiren) and 2 beta- ... Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) increase plasma renin activity ( ... Angiotensin-Converting Enzyme Inhibitors / administration & dosage * Angiotensin-Converting Enzyme Inhibitors / adverse effects ...
The brain RAS system exhibits pleiotropic properties such as neuroprotection and cognition along with regulation of blood ... The review summarizes the recent advances in the brain RAS system highlighting its significance in pathophysiology and ... angiotensin (Ang), and specific receptors (ATR). AGT acts as the precursor molecule for Ang peptides—I, II, III, and IV ... is the part of the endocrine system that plays a prime role in the control of essential hypertension. Since the discovery of ...
The renin-angiotensin system (RAS) is a major hormonal autocrine/paracrine system that under normal conditions contributes to ... Suppression of the Renin-Angiotensin-Aldosterone System. "It is not the answers that enlighten, but the questions." - Ionesco ... Discuss the role of the renin-angiotensin-Aldosterone system (RAS) in development of hypertension ... Discuss the recent data of the blood pressure-lowering effects achieved through renin inhibition. ...
Renin-Angiotensin-Aldosterone System in Pregnancy. Normal pregnancy is associated with many changes in the renin-angiotensin- ... Blood pressure, the renin-aldosterone system and sex steroids throughout normal pregnancy. Am J Med. 1980 Jan. 68(1):97-104. [ ... Plasma renin levels should be decreased in patients with primary hyperaldosteronism. In a healthy pregnancy, plasma renin ... In pregnant patients, prolonged upright posture results in a modest increase in plasma renin activity. If the renin activity ...
The antagonists of the renin-angiotensin-aldosterone system (RAAS) have been shown to interfere with angiotensin converting ... Inhibitors of the renin-angiotensin-aldosterone system and CoViD-19-affected patients: A two-faced Janus?. ... Inhibitors of the renin-angiotensin-aldosterone system and CoViD-19-affected patients: A two-faced Janus? ... Inhibitors of the renin-angiotensin-aldosterone system and CoViD-19-affected patients: A two-faced Janus? ...
Renin-angiotensin-aldosterone system genes and nonarteritic anterior ischemic optic neuropathy. Sofia Markoula,1 Sotirios ... Jiang X, Sheng H, Li J, Xun P, Cheng Y, Huang J, Xiao H, Zhan Y. Association between renin-angiotensin system gene polymorphism ... The renin-angiotensin system genes exhibit three common polymorphisms: the insertion/deletion (I/D) polymorphism of the ... NAION and control groups were compared in regard to the prevalence of renin-angiotensin-aldosterone system polymorphisms, and ...
Renin-angiotensin-aldosterone system-Operative pathway regulating vascular volume, salt and water retention. ... Renin is the first enzyme in the renin-angiotensin-aldosterone system.. Renin cleaves angiotensinogen to angiotensin I, which ... Blockade of the renin-angiotensin-aldosterone system (RASS) with angiotensin-converting enzyme inhibition or angiotensin ... Progressive activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system contributes to chronic ...
Eight SNPs of three RAS genes (angiotensinogen, ,i,AGT,/i,; angiotensin-converting enzyme, ,i,ACE,/i,; angiotensin II type 1 ... of renin-angiotensin system (RAS) genes are associated with hypertension (HT) but most of them are focusing on single locus ... The renin-angiotensin system (RAS) represents a critical endocrine regulator for maintaining blood pressure and blood fluid ... C.-T. Tsai, J.-J. Hwang, M. D. Ritchie et al., "Renin-angiotensin system gene polymorphisms and coronary artery disease in a ...
Activation of tissue-specific gene expression of the components of the renin-angiotensin system (RAS) in humans may play an ... Gene expression of the renin-angiotensin system in human tissues. Quantitative analysis by the polymerase chain reaction.. ... Gene expression of the renin-angiotensin system in human tissues. Quantitative analysis by the polymerase chain reaction.. ... 0.2 pg renin/micrograms total RNA), adrenal gland (1.15 +/- 0.15 pg renin/micrograms total RNA), placenta (0.7 +/- 0.1 pg renin ...
... and angiotensin II receptor blocker AT-1 (ARBs) in reducing the systemic hypertension (SH) is widely known. However their ... The effectiveness of angiotensin-converting enzyme inhibitors (ACEIs) ... Selected Chapters from the Renin-Angiot... Edited by Aleksandar Kibel. Selected Chapters from the Renin-Angiotensin System. ... The Intratubular and Intracrine Renin-Angiotensin System in the Proximal Tubules of the Kidney and Its Roles in Angiotensin II- ...
10 Endogenous and exogenous loading of extracellular vesicles for therapeutic delivery of renin-angiotensin system peptides in ... 10 Endogenous and exogenous loading of extracellular vesicles for therapeutic delivery of renin-angiotensin system peptides in ... The counter-regulatory RAS axis peptide Angiotensin 1-7 [Ang-(1-7)] inhibits cardiomyocyte hypertrophy. EVs were purified from ... Introduction The RAS peptide angiotensin II (AngII) mediates cardiac hypertrophy. ...
Decongestion strategies and renin-angiotensin-aldosterone system activation in acute heart failure. ... OBJECTIVES: The purpose of this study was to assess the relationship between biomarkers of renin-angiotensin-aldosterone system ... Decongestion strategies and renin-angiotensin-aldosterone system activation in acute heart failure. JACC Heart Fail, 3(2). pp. ... We assessed the relationship between 2 markers of RAAS activation (plasma renin activity [PRA] and aldosterone) from baseline ...
Protective arms of the renin-angiotensin-system in neurological disease. Colin Sumners, Masatsugu Horiuchi, Robert Edward ... title = "Protective arms of the renin-angiotensin-system in neurological disease",. abstract = "In recent years it has been ... firmly established that apart from the classic renin-angiotensin system (RAS) comprising angiotensin (Ang) II, angiotensin ... Protective arms of the renin-angiotensin-system in neurological disease. / Sumners, Colin; Horiuchi, Masatsugu; Widdop, Robert ...
Co-trimoxazole and sudden death in patients receiving inhibitors of renin-angiotensin system: population based study. BMJ 2014; ... Cotrimoxazole is associated with sudden death in older patients receiving inhibitors of renin-angiotensin system ... Cotrimoxazole is associated with sudden death in older patients receiving inhibitors of renin-angiotensin system ... ACE inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) are commonly prescribed to older patients with hypertension, ...
... renin-angiotensin system; RASi, renin-angiotensin system inhibitor. ... Inhibition of the renin-angiotensin system causes concentric hypertrophy of renal arterioles in mice and humans. Hirofumi ... Inhibitors of the renin-angiotensin system (RAS) are widely used to treat hypertension. Using mice harboring fluorescent cell ... Renin-angiotensin-aldosterone (RAAS): The ubiquitous system for homeostasis and pathologies. Biomed Pharmacother. 2017;94(raas ...
... plasma renin activity (PRA), and aldosterone up to 6h after furosemide injection. Urinary electrolyte excretion was also ... Interactions between sodium and calcium regulating systems are poorly characterized but clinically important. Parathyroid ... Mineral metabolism ; Calcium-sensing receptor ; Renin-angiotensin-aldosterone system ; Cinacalcet ; Furosemide. OAI-PMH ... Furosemide stimulation of parathormone in humans: role of the calcium-sensing receptor and the renin-angiotensin system Muller ...
This investigation has examined a possible role for the renin-angiotensin system as well as body mass and insulin values in ... but that in normal weight hypertensives the renin-angiotensin system may play the major role. ... LVM in lean patients correlated significantly with plasma renin activity (PRA), plasma aldosterone, BMI and systolic BP; but ... This investigation has examined a possible role for the renin-angiotensin system as well as body mass and insulin values in ...
To explore the association between use of renin-angiotensin-system inhibitors (RASi) and beta-blockers, with mortality/ ... To explore the association between use of renin-angiotensin-system inhibitors (RASi) and beta-blockers, with mortality/ ... Does Heterogeneity Exist in Treatment Associations with Renin-Angiotensin-System Inhibitors or Beta-blockers According to ...
renin-angiotensin-aldosterone system (RAAS). prorenin. renin angiotensin converting enzyme 2. angiotensin-1-7. angiotensin II. ... renin-angiotensin-aldosterone system (RAAS); prorenin; renin angiotensin converting enzyme 2; angiotensin-1-7; angiotensin II; ... The renin-angiotensin-aldosterone system (RAAS) - new pathogenetic and therapeutic aspects Part. I. Prorenin and renin and its ... The renin-angiotensin-aldosterone system (RAAS) - new pathogenetic and therapeutic aspects Part. I. Prorenin and renin and its ...
Using a Systems Biology Approach to Explore Hypotheses Underlying Clinical Diversity of the Renin Angiotensin System and the ... Systemic Renin-Angiotensin-System. Fulden Buyukozturk on 10 Oct 2018 (Edited on 11 Jun 2020) ... This project presents SimBiology model implementation of the systemic Renin-Angiotensin-System that was first developed by Lo ... Angiotensin II and Angiotensin IV. Key pathway effects are triggered by the association of Angiotensin II with the AT1-Receptor ...
The RAAS is a hormone system that regulates blood pressure and fluid balance. This article shall discuss the RAAS and its ... The Renin-Angiotensin-Aldosterone System (RAAS) is a hormone system within the body that is essential for the regulation of ... The Renin-Angiotensin-Aldosterone System (RAAS) is a hormone system within the body that is essential for the regulation of ... The system is mainly comprised of the three hormones renin, angiotensin II, and aldosterone. Primarily it is regulated by the ...
... is an angiotensin converting enzyme (ACE) inhibitor used to treat and lower high blood pressure. Common side effects of Mavik ... Dual Blockade Of The Renin-Angiotensin System (RAS). Dual blockade of the RAS with angiotensin receptor blockers, ACE ... Angiotensin II is formed by ACE. Mavik is an inhibitor of ACE and blocks the formation of angiotensin II thereby lowering blood ... Angiotensin II is a chemical substance made in the body that causes the muscles in the walls of arteries and veins to contract ...
ATC Group: C09 Agents acting on the renin-angiotensin system. The World Health Organizations ATC classification organizes ...
Interaction with Renin-Angiotensin-Aldosterone System Inhibitors. Drugs that inhibit the renin-angiotensin-aldosterone system ( ... may produce potassium retention by reducing renal synthesis of prostaglandin E and impairing the renin-angiotensin system. ... RAAS) including angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), spironolactone, ... An active ion transport system maintains this gradient across the plasma membrane. ...
Get assignment sample for G-Protein Coupled Receptors of The Renin-Angiotensin System on My Assignment Services. Download now! ... known as the renin-angiotensin system or RAS distributes three different types of GCPRs - angiotensin type-1, angiotensin type- ... References for G-Protein Coupled Receptors of The Renin-Angiotensin System. Jara, Z. P., Singh, K. D., Unal, H., Desnoyer, R., ... Evidence suggests that components of the renin-angiotensin system, namely AngIIand Ang1-7, are harmful and protective against ...
Basic Mechanisms and Pre-clinical Evidence In Terms of Cross-talk Between Statin and the Renin-angiotensin System. Statins ... Clinical Evidences of Cross-talk Between Statins and the Renin-angiotensin System. We reported additive beneficial effects of ... Clinical Perspectives of Cross-talk Between Statins and the Renin-angiotensin System. Impaired endothelial vasodilation is ... Cross-talk Between Statins and the Renin-angiotensin System Seung Hwan Han ...
Inhibition of the renin-angiotensin-aldosterone system (RAAS) is broadly recommended in many nephrological guidelines to ... Inhibition of the renin-angiotensin-aldosterone system (RAAS) is broadly recommended in many nephrological guidelines to ... Randomized Controlled Trials on Renin Angiotensin Aldosterone System Inhibitors in Chronic Kidney Disease Stages 3-5: Are They ... Randomized Controlled Trials on Renin Angiotensin Aldosterone System Inhibitors in Chronic Kidney Disease Stages 3-5: Are They ...

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