Potassium Deficiency
Hypokalemia
Potassium
Sexual Infantilism
Adrenal Hyperplasia, Congenital
Steroid 21-Hydroxylase
Disorders of Sex Development
17-alpha-Hydroxyprogesterone
Antihypertensive Agents
Monocytic cell necrosis is mediated by potassium depletion and caspase-like proteases. (1/127)
Apoptosis is a physiological cell death that culminates in mitochondrial permeability transition and the activation of caspases, a family of cysteine proteases. Necrosis, in contrast, is a pathological cell death characterized by swelling of the cytoplasm and mitochondria and rapid plasma membrane disruption. Necrotic cell death has long been opposed to apoptosis, but it now appears that both pathways involve mitochondrial permeability transition, raising the question of what mediates necrotic cell death. In this study, we investigated mechanisms that promote necrosis induced by various stimuli (Clostridium difficile toxins, Staphylococcus aureus alpha toxin, ouabain, nigericin) in THP-1 cells, a human monocytic cell line, and in monocytes. All stimuli induced typical features of necrosis and triggered protease-mediated release of interleukin-1beta (IL-1beta) and CD14 in both cell types. K+ depletion was actively implicated in necrosis because substituting K+ for Na+ in the extracellular medium prevented morphological features of necrosis and IL-1beta release. N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone, a broad-spectrum caspase inhibitor, prevented morphological features of necrosis, plasma membrane destruction, loss of mitochondrial membrane potential, IL-1beta release, and CD14 shedding induced by all stimuli. Thus, in monocytic cells, necrosis is a cell death pathway mediated by passive K+ efflux and activation of caspase-like proteases. (+info)H+-K+-ATPases: regulation and role in pathophysiological states. (2/127)
Molecular cloning experiments have identified the existence of two H+-K+-ATPases (HKAs), colonic and gastric. Recent functional and molecular studies indicate the presence of both transporters in the kidney, which are presumed to mediate the exchange of intracellular H+ for extracellular K+. On the basis of these studies, a picture is evolving that indicates differential regulation of HKAs at the molecular level in acid-base and electrolyte disorders. Of the two transporters, gastric HKA is expressed constitutively along the length of the collecting duct and is responsible for H+ secretion and K+ reabsorption under normal conditions and may be stimulated with acid-base perturbations and/or K+ depletion. This regulation may be species specific. To date there are no data to indicate that the colonic HKA (HKAc) plays a role in H+ secretion or K+ reabsorption under normal conditions. However, HKAc shows adaptive regulation in pathophysiological conditions such as K+ depletion, NaCl deficiency, and proximal renal tubular acidosis, suggesting an important role for this exchanger in potassium, HCO-3, and sodium (or chloride) reabsorption in disease states. The purpose of this review is to summarize recent functional and molecular studies on the regulation of HKAs in physiological and pathophysiological states. Possible signals responsible for regulation of HKAs in these conditions will be discussed. Furthermore, the role of these transporters in acid-base and electrolyte homeostasis will be evaluated in the context of genetically altered animals deficient in HKAc. (+info)Acute effect of hydrochlorothiazide on renal calcium and magnesium handling in postmenopausal women. (3/127)
A single 50 mg dose of hydrochlorothiazide (HCTZ) decreases the urinary excretion of calcium (U(Ca)V), clearance (C(Ca)) and fractional excretion (FE(Ca)) of calcium. This is accompanied by an increase of total calcium and ionized calcium (Ca2+) concentrations in the serum. On the other hand, HCTZ increases fractional excretion of magnesium (FE(Mg)) and decreases serum Mg2+ concentrations. Moreover, HCTZ decreases markedly clearance of phosphate (C(Pi)) and fractional excretion of phosphate (FE(Pi)) and increases serum phosphate (Pi) concentrations in healthy postmenopausal women. It is concluded that intrinsic renal cellular control promptly uncouples calcium and magnesium tubular reabsorption even without K+ depletion. (+info)Cellular origin and hormonal regulation of K(+)-ATPase activities sensitive to Sch-28080 in rat collecting duct. (4/127)
Rat collecting ducts exhibit type I or type III K(+)-ATPase activities when animals are fed a normal (NK) or a K(+)-depleted diet (LK). This study aimed at determining functionally the cell origin of these two K(+)-ATPases. For this purpose, we searched for an effect on K(+)-ATPases of hormones that trigger cAMP production in a cell-specific fashion. The effects of 1-deamino-8-D-arginine vasopressin (dD-AVP), calcitonin, and isoproterenol in principal cells, alpha-intercalated cells, and beta-intercalated cells of cortical collecting duct (CCD), respectively, and of dD-AVP and glucagon in principal and alpha-intercalated cells of outer medullary collecting duct (OMCD), respectively, were examined. In CCDs, K(+)-ATPase was stimulated by calcitonin and isoproterenol in NK rats (type I K(+)-ATPase) and by dD-AVP in LK rats (type III K(+)-ATPase). In OMCDs, dD-AVP and glucagon stimulated type III but not type I K(+)-ATPase. These hormone effects were mimicked by the cAMP-permeant analog dibutyryl-cAMP. In conclusion, in NK rats, cAMP stimulates type I K(+)-ATPase activity in alpha- and beta-intercalated CCD cells, whereas in LK rats it stimulates type III K(+)-ATPase in principal cells of both CCD and OMCD and in OMCD intercalated cells. (+info)Short-term K(+) deprivation provokes insulin resistance of cellular K(+) uptake revealed with the K(+) clamp. (5/127)
We aimed to test the feasibility of quantifying insulin action on cellular K(+) uptake in vivo in the conscious rat by measuring the exogenous K(+) infusion rate needed to maintain constant plasma K(+) concentration ([K(+)]) during insulin infusion. In this "K(+) clamp" the K(+) infusion rate required to clamp plasma [K(+)] is a measure of insulin action to increase net plasma K(+) disappearance. K(+) infusion rate required to clamp plasma [K(+)] was insulin dose dependent. Renal K(+) excretion was not significantly affected by insulin at a physiological concentration ( approximately 90 microU/ml, P > 0.05), indicating that most of insulin-mediated plasma K(+) disappearance was due to K(+) uptake by extrarenal tissues. In rats deprived of K(+) for 2 days, plasma [K(+)] fell from 4.2 to 3.8 mM, insulin-mediated plasma glucose clearance was normal, but insulin-mediated plasma K(+) disappearance decreased to 20% of control, even though there was no change in muscle Na-K-ATPase activity or expression, which is believed to be the main K(+) uptake route. After 10 days K(+) deprivation, plasma [K(+)] fell to 2.9 mM, insulin-mediated K(+) disappearance decreased to 6% of control (glucose clearance normal), and there were 50% decreases in Na-K-ATPase activity and alpha2-subunit levels. In conclusion, the present study proves the feasibility of the K(+) clamp technique and demonstrates that short-term K(+) deprivation leads to a near complete insulin resistance of cellular K(+) uptake that precedes changes in muscle sodium pump expression. (+info)Magnesium transport in the renal distal convoluted tubule. (6/127)
The distal tubule reabsorbs approximately 10% of the filtered Mg(2+), but this is 70-80% of that delivered from the loop of Henle. Because there is little Mg(2+) reabsorption beyond the distal tubule, this segment plays an important role in determining the final urinary excretion. The distal convoluted segment (DCT) is characterized by a negative luminal voltage and high intercellular resistance so that Mg(2+) reabsorption is transcellular and active. This review discusses recent evidence for selective and sensitive control of Mg(2+) transport in the DCT and emphasizes the importance of this control in normal and abnormal renal Mg(2+) conservation. Normally, Mg(2+) absorption is load dependent in the distal tubule, whether delivery is altered by increasing luminal Mg(2+) concentration or increasing the flow rate into the DCT. With the use of microfluorescent studies with an established mouse distal convoluted tubule (MDCT) cell line, it was shown that Mg(2+) uptake was concentration and voltage dependent. Peptide hormones such as parathyroid hormone, calcitonin, glucagon, and arginine vasopressin enhance Mg(2+) absorption in the distal tubule and stimulate Mg(2+) uptake into MDCT cells. Prostaglandin E(2) and isoproterenol increase Mg(2+) entry into MDCT cells. The current evidence indicates that cAMP-dependent protein kinase A, phospholipase C, and protein kinase C signaling pathways are involved in these responses. Steroid hormones have significant effects on distal Mg(2+) transport. Aldosterone does not alter basal Mg(2+) uptake but potentiates hormone-stimulated Mg(2+) entry in MDCT cells by increasing hormone-mediated cAMP formation. 1,25-Dihydroxyvitamin D(3), on the other hand, stimulates basal Mg(2+) uptake. Elevation of plasma Mg(2+) or Ca(2+) inhibits hormone-stimulated cAMP accumulation and Mg(2+) uptake in MDCT cells through activation of extracellular Ca(2+)/Mg(2+)-sensing mechanisms. Mg(2+) restriction selectively increases Mg(2+) uptake with no effect on Ca(2+) absorption. This intrinsic cellular adaptation provides the sensitive and selective control of distal Mg(2+) transport. The distally acting diuretics amiloride and chlorothiazide stimulate Mg(2+) uptake in MDCT cells acting through changes in membrane voltage. A number of familial and acquired disorders have been described that emphasize the diversity of cellular controls affecting renal Mg(2+) balance. Although it is clear that many influences affect Mg(2+) transport within the DCT, the transport processes have not been identified. (+info)Contribution of an electrogenic sodium pump to membrane potential in mammalian skeletal muscle fibres. (7/127)
1. Relationship between the resting membrane potential and the changes in the intraceullar Na and K concentrations ([Na]i and [K]i) was studied in 'Na-loaded' and K-depleted' soleus (SOL) muscles of rats which had fed a K-free diet for 40 and more days. 2. The extracellular space of the muscles was not significantly different between normal and K-deficient rats. The inulin space in both the 'fresh' and Na-rich' muscles can be determined by the same function relating the space to the muscle weight. 3. Presence of 2-5-15 mM-K in the recovery solution hyperpolarized the 'Na-rich' muscul fibres at the beginning of recovery. The hyperpolarized membrane potential exceeded, beyond the measured potential of 'fresh' muscle fibres, the theoretical potential derived from the ionic theory, or even beyond Ek. Then, the measured membrane potential declined progressively during the immersion in a recovery solution and returned to the steady-state value When a considerable Na extrusion and K uptake took place, the measured membrane potential became equal to Ek. 4.he maximal hyperpolarization occurring immediately after immersion in the recovery solution became smaller and had a shorter duration when increasing the external K concentration ([K]o) from 2-5 to 15mM. 5. The K-sensitive hyperpolarization was completely abolished on exposure to 0mM [K]o, on cooling to ca. 4 degrees C, and in the presence of oubain (10(-4) M). The inhibitory effects were reversed on returning to the control conditions. The membrane potential obtained after inhibition of the electrogenic Na-pump with cooling or ouabain agrees well with that predicted by the 'constant-field' equation. 7. The external Cl ions had a short-circuiting effect on the electrogenic Na-pumping activated on adding K ions. 8. The replacement of Na ions in a recovery solution with Li ions resulted in a faster rate of depolarization from the maximal hyperpolarizationp. It is concluded that the resting membrane potential of 'Na-loaded' and 'K-depleted' SOL muscle fibres is the sum of an ionic diffusion potential predicted by either the Nernst equation or the constant-field equation and of the potential produced by an electrogenic Na-pump. (+info)Glycosphingolipids modulate renal phosphate transport in potassium deficiency. (8/127)
BACKGROUND: Potassium (K) deficiency (KD) and/or hypokalemia have been associated with disturbances of phosphate metabolism. The purpose of the present study was to determine the cellular mechanisms that mediate the impairment of renal proximal tubular Na/Pi cotransport in a model of K deficiency in the rat. METHODS: K deficiency in the rat was achieved by feeding rats a K-deficient diet for seven days, which resulted in a marked decrease in serum and tissue K content. RESULTS: K deficiency resulted in a marked increase in urinary Pi excretion and a decrease in the V(max) of brush-border membrane (BBM) Na/Pi cotransport activity (1943 +/- 95 in control vs. 1184 +/- 99 pmol/5 sec/mg BBM protein in K deficiency, P < 0.02). Surprisingly, the decrease in Na/Pi cotransport activity was associated with increases in the abundance of type I (NaPi-1), and type II (NaPi-2) and type III (Glvr-1) Na/Pi protein. The decrease in Na/Pi transport was associated with significant alterations in BBM lipid composition, including increases in sphingomyelin, glucosylceramide, and ganglioside GM3 content and a decrease in BBM lipid fluidity. Inhibition of glucosylceramide synthesis resulted in increases in BBM Na/Pi cotransport activity in control and K-deficient rats. The resultant Na/Pi cotransport activity in K-deficient rats was the same as in control rats (1148 +/- 52 in control + PDMP vs. 1152 +/- 61 pmol/5 sec/mg BBM protein in K deficiency + PDMP). These changes in transport activity occurred independent of further changes in BBM NaPi-2 protein or renal cortical NaPi-2 mRNA abundance. CONCLUSION: K deficiency in the rat causes inhibition of renal Na/Pi cotransport activity by post-translational mechanisms that are mediated in part through alterations in glucosylceramide content and membrane lipid dynamics. (+info)Potassium deficiency, also known as hypokalemia, is a condition characterized by low levels of potassium (
Hypokalemia is a medical condition characterized by abnormally low potassium levels in the blood, specifically when the concentration falls below 3.5 milliequivalents per liter (mEq/L). Potassium is an essential electrolyte that helps regulate heart function, nerve signals, and muscle contractions.
Hypokalemia can result from various factors, including inadequate potassium intake, increased potassium loss through the urine or gastrointestinal tract, or shifts of potassium between body compartments. Common causes include diuretic use, vomiting, diarrhea, certain medications, kidney diseases, and hormonal imbalances.
Mild hypokalemia may not cause noticeable symptoms but can still affect the proper functioning of muscles and nerves. More severe cases can lead to muscle weakness, fatigue, cramps, paralysis, heart rhythm abnormalities, and in rare instances, respiratory failure or cardiac arrest. Treatment typically involves addressing the underlying cause and replenishing potassium levels through oral or intravenous (IV) supplementation, depending on the severity of the condition.
Potassium is a essential mineral and an important electrolyte that is widely distributed in the human body. The majority of potassium in the body (approximately 98%) is found within cells, with the remaining 2% present in blood serum and other bodily fluids. Potassium plays a crucial role in various physiological processes, including:
1. Regulation of fluid balance and maintenance of normal blood pressure through its effects on vascular tone and sodium excretion.
2. Facilitation of nerve impulse transmission and muscle contraction by participating in the generation and propagation of action potentials.
3. Protein synthesis, enzyme activation, and glycogen metabolism.
4. Regulation of acid-base balance through its role in buffering systems.
The normal serum potassium concentration ranges from 3.5 to 5.0 mEq/L (milliequivalents per liter) or mmol/L (millimoles per liter). Potassium levels outside this range can have significant clinical consequences, with both hypokalemia (low potassium levels) and hyperkalemia (high potassium levels) potentially leading to serious complications such as cardiac arrhythmias, muscle weakness, and respiratory failure.
Potassium is primarily obtained through the diet, with rich sources including fruits (e.g., bananas, oranges, and apricots), vegetables (e.g., leafy greens, potatoes, and tomatoes), legumes, nuts, dairy products, and meat. In cases of deficiency or increased needs, potassium supplements may be recommended under the guidance of a healthcare professional.
Sexual infantilism, also known as paraphilic infantilism or autonepiophilia, is a psychological condition where an individual has a persistent and intense sexual interest in role-playing as a baby or small child, often involving the use of diapers, clothing, and other props. This behavior is considered a paraphilia when it interferes with normal social functioning or causes distress to the individual or others. It's important to note that this behavior does not involve sexual contact with children, but rather derives sexual pleasure from acting like one.
It's worth mentioning that this condition is still not well understood and more research is needed to fully grasp its prevalence, causes, and treatment options. As always, if you or someone else is struggling with any kind of sexual disorder or distress, it's recommended to seek help from a mental health professional or medical doctor who specializes in sexual disorders.
Congenital Adrenal Hyperplasia (CAH) is a group of inherited genetic disorders that affect the adrenal glands, which are triangular-shaped glands located on top of the kidneys. The adrenal glands are responsible for producing several essential hormones, including cortisol, aldosterone, and androgens.
CAH is caused by mutations in genes that code for enzymes involved in the synthesis of these hormones. The most common form of CAH is 21-hydroxylase deficiency, which affects approximately 90% to 95% of all cases. Other less common forms of CAH include 11-beta-hydroxylase deficiency and 3-beta-hydroxysteroid dehydrogenase deficiency.
The severity of the disorder can vary widely, depending on the degree of enzyme deficiency. In severe cases, the lack of cortisol production can lead to life-threatening salt wasting and electrolyte imbalances in newborns. The excess androgens produced due to the enzyme deficiency can also cause virilization, or masculinization, of female fetuses, leading to ambiguous genitalia at birth.
In milder forms of CAH, symptoms may not appear until later in childhood or even adulthood. These may include early puberty, rapid growth followed by premature fusion of the growth plates and short stature, acne, excessive hair growth, irregular menstrual periods, and infertility.
Treatment for CAH typically involves replacing the missing hormones with medications such as hydrocortisone, fludrocortisone, and/or sex hormones. Regular monitoring of hormone levels and careful management of medication doses is essential to prevent complications such as adrenal crisis, growth suppression, and osteoporosis.
In severe cases of CAH, early diagnosis and treatment can help prevent or minimize the risk of serious health problems and improve quality of life. Genetic counseling may also be recommended for affected individuals and their families to discuss the risks of passing on the disorder to future generations.
Steroid 21-hydroxylase, also known as CYP21A2, is a crucial enzyme involved in the synthesis of steroid hormones in the adrenal gland. Specifically, it catalyzes the conversion of 17-hydroxyprogesterone to 11-deoxycortisol and progesterone to deoxycorticosterone in the glucocorticoid and mineralocorticoid pathways, respectively.
Deficiency or mutations in this enzyme can lead to a group of genetic disorders called congenital adrenal hyperplasia (CAH), which is characterized by impaired cortisol production and disrupted hormonal balance. Depending on the severity of the deficiency, CAH can result in various symptoms such as ambiguous genitalia, precocious puberty, sexual infantilism, infertility, and increased risk of adrenal crisis.
Disorders of Sex Development (DSD) are a group of conditions that occur when there is a difference in the development and assignment of sex characteristics. These differences may be apparent at birth, at puberty, or later in life. DSD can affect chromosomes, gonads, genitals, or secondary sexual characteristics, and can result from genetic mutations or environmental factors during fetal development.
DSDs were previously referred to as "intersex" conditions, but the term "Disorders of Sex Development" is now preferred in medical settings because it is more descriptive and less stigmatizing. DSDs are not errors or abnormalities, but rather variations in human development that require sensitive and individualized care.
The diagnosis and management of DSD can be complex and may involve a team of healthcare providers, including endocrinologists, urologists, gynecologists, psychologists, and genetic counselors. Treatment options depend on the specific type of DSD and may include hormone therapy, surgery, or other interventions to support physical and emotional well-being.
17-α-Hydroxyprogesterone is a naturally occurring hormone produced by the adrenal glands and, in smaller amounts, by the ovaries and testes. It is an intermediate in the biosynthesis of steroid hormones, including cortisol, aldosterone, and sex hormones such as testosterone and estrogen.
In a medical context, 17-α-Hydroxyprogesterone may also refer to a synthetic form of this hormone that is used in the treatment of certain medical conditions. For example, a medication called 17-alpha-hydroxyprogesterone caproate (17-OHP) is used to reduce the risk of preterm birth in women who have previously given birth prematurely. It works by suppressing uterine contractions and promoting fetal lung maturity.
It's important to note that 17-alpha-Hydroxyprogesterone should only be used under the supervision of a healthcare provider, as it can have side effects and may interact with other medications.
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.
Pregnanetriol is not a medication, but rather a metabolite of the hormone progesterone. It is a steroid compound that is produced in the body and can be detected in urine. Pregnanetriol is often used as a biomarker to help diagnose certain medical conditions related to steroid hormone metabolism, such as congenital adrenal hyperplasia (CAH). In these cases, abnormal levels of pregnanetriol in the urine can indicate an enzyme deficiency that affects the production or breakdown of steroid hormones.