Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In guinea pigs, administration of digitoxin (0.3 mg/kg s.c. for 7-24 days) causes an increase in activity of the (Na+ + K+)-ATPase of the heart. The plasma K+ level and the K+ content of the heart muscle of these animals remains unchanged and there is no significant alteration in the digitoxin toxicity compared to controls. In guinea pigs with potassium deficiency produced by a potassium deficient diet for 12 days, there is a related increase of the (Na+ + K+)-ATPase. The plasma K+ level of these animals is diminished while the K+ content in the heart muscle remains unchanged the toxicity of digitoxin is enhanced. In both test groups the increase in the (Na+ + K+)-ATPase activity is limited to enzymes from heart muscle, those from brain or kidney remaining unaffected. This increase in activity seems to be the result of an adaptive enzyme induction.
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PMID:Increase in the (Na+ + K+)-ATPase activity in heart muscle after chronic treatment with digitoxin or potassium deficient diet. 13 55

The mechanisms responsible for renal potassium (K) conservation during dietary potassium deficiency are poorly understood. This study was undertaken to investigate the time course of potassium conservation as well as the roles of distal sodium (Na) delivery, the distal delivery or sodium plus a nonpermeable anion, mineralocorticoid hormone, renal tissue potassium content, and Na-K-ATPase activity in renal potassium conservation. After 72 hours of a low-potassium diet, basal potassium excretion was negligible. After 24 hours, and even more so after 72 hours of potassium restriction, the kaliuretic response to increasing distal delivery of sodium or sodium plus a nonpermeable anion was impaired. After 24 hours of a low-potassium diet, plasma aldosterone levels fell from 180 +/- 25 to 32 +/- 9 pg/ml (P less than 0.001). Mineralocorticoid hormone given in the first 24 hours of a low-potassium diet resulted in a greater potassium loss (1564 +/- 125 muEq) than it did in controls on the same diet not receiving mineralocorticoid hormone (1032 +/- 83 muEq, P less than 0.005). In contrast, after 72 hours of diet, large doses of mineralocorticoid hormone failed to cause a kaliuresis in either anesthetized or conscious rats. After both 24 and 72 hours, outer medullary Na-K-ATPase was increased. At 72 hours, cortical, medullary, and papillary tissue potassium concentrations were significantly depressed. Acute administration of potassium repleted tissue potassium levels and restored basal and saline-stimulated potassium excretion to normal. Although potassium excretion was markedly depressed after 24 hours of the low-potassium diet, 42K microinjection studies of the distal nephron did not suggest any increase in potassium reabsorption. Following 72 hours of diet, potassium reabsorption increased significantly from 26 +/- 2% to 41 +/- 2% (P less than 0.001). We conclude that renal potassium conservation is at first primarily related to a decrease in potassium secretion, which is most likely mediated by falling levels of mineralocorticoid hormone. After 72 hours of the potassium-deficient diet, however, potassium conservation becomes independent of mineralocorticoid hormone, distal delivery of sodium, and Na-K-ATPase. The decreased tissue potassium content appears to be the primary mediator of both the increase in potassium reabsorption by the distal nephron and of renal potassium conservation at this time.
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PMID:Mechanism of renal potassium conservation in the rat. 22 34

Lowering the extracellular K+ content from 6 to 0.6 mM causes a rise, and elevation from 6 to 8.5 mM a fall of 45Ca++ efflux from the vascular smooth muscle cells of the arteria carotis communis of cattle. In contrast, a level of 17 mM K+ has no influence. Removal of extracellular calcium does not block these effects. 10(-4) M ouabain also induces a rise in Ca++ efflux, additional potassium reduction then being without effect; 10(-9) M ouabain is of no influence. The 45Ca++ efflux kinetics correlates with the activity of the isolated Na,K-ATPase. Tonus increases of the vascular strips by 10(-4) M ouabain and potassium deficiency cannot be blocked by 4 mM lanthanum or removal of extracellular calcium. Unlike sodium, potassium stimulates the active Ca++ binding and the activity of the Ca-ATPase of the microsomal fraction. The ative Ca++ binding of the mitochondria is stimulated by both ions. It is postulated that the activity of the plasma membrane Na,K-pump is able to regulate the tonus of big arteries through alteration of Ca++ storage processes.
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PMID:Na,K-ATPase in excitation-contraction coupling of vascular smooth muscle from cattle. 22 70

The present study was undertaken to investigate whether or not potassium deficiency influences N-ethylmaleimide (NEM)-sensitive ATPase in the distal nephron segments of the rat. One group of animals was fed a low-K diet, whereas the normal K-group was given the same diet after supplementation with KCl. The nephron segments examined were: the medullary and cortical thick ascending limbs, the distal convoluted tubule, and the cortical, outer and inner medullary collecting ducts. NEM-sensitive ATPase activity in microdissected segments was measured by a fluorometric microassay. The plasma K+ concentration in the low-K group was 3.1 +/- 0.3 mEq/l compared with 4.2 +/- 0.1 mEq/l in the normal-K group. NEM-sensitive ATPase activity in the outer medullary collecting duct of low-K diet animals was significantly greater than in normal-K animals. There was no significant difference in NEM-sensitive ATPase activity between the two groups of animals in the other nephron segments examined. It is suggested that NEM-sensitive H-ATPase activity in the outer medullary collecting duct is modulated by the potassium status of the animal.
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PMID:Effects of low-potassium diet on N-ethylmaleimide-sensitive ATPase in the distal nephron segments. 169 Sep 6

Potassium depletion can potentiate several experimental models of acute renal failure. It causes renal vasoconstriction, probably under the influence of vasoconstrictor prostaglandins and angiotensin II, and causes a reduction in vasodilatory prostaglandins. Aminoglycoside nephrotoxicity in experimental animals and in man causes a reduction in serum potassium and in animals it enhances the functional and histological damage produced by aminoglycosides. Chronic potassium loading protects against mercuric chloride, uranyl nitrate, and gentamicin models of acute renal failure. In the gentamicin model, protection is associated with a stimulation of renal cortical Na-K-ATPase activity and a reduction in the level of gentamicin accumulated in cortical tissue. In the clinical setting, potassium deficiency should be avoided in patients at risk for acute renal failure. However, potassium loading should also be avoided, since a falling glomerular filtration rate in the presence of a potassium load could result in potentially serious hyperkalemia.
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PMID:Role of potassium in the pathogenesis of acute renal failure. 175 17

Contracting muscle cells release K ions into their surrounding interstitial fluid, and some of these ions, in turn, enter venous plasma. Thereby, intense or exhaustive exercise may result in hyperkalemia and potentially dangerous cardiotoxicity. Training not only reduces hyperkalemia produced by exercise but in addition, highly conditioned, long-distance runners may show resting hypokalemia that is not caused by K deficiency. To examine the factors underlying these changes, dogs were studied before and after 6 wk of training induced by running on the treadmill. Resting serum [K] fell from 4.2 +/- 0.2 to 3.9 +/- 0.3 meq/liter (P less than 0.001), muscle intracellular [K] rose from 139 +/- 7 to 148 +/- 14 meq/liter (P less than 0.001), and directly measured muscle cell membrane potential (Em) in vivo rose from -92 +/- 5 to -103 +/- 5 mV (P less than 0.001). Before training, resting Em of isolated intercostal muscle in vitro was -87 +/- 5 mV, and after incubation in 10(-4) M ouabain, Em fell to -78 +/- 5 mV. After training, resting Em of intercostal muscle rose to -95 +/- 4, but fell to -62 +/- 4 mV during incubation in 10(-4) M ouabain. The measured value for the Em was not completely explained by the increased ratio of intracellular to extracellular [K] or by the potassium diffusion potential. Skeletal muscle sarcolemmal Na,K-ATPase activity (microM inorganic phosphate mg-1 protein h-1) increased from 0.189 +/- 0.028 to 0.500 +/- 0.076 (P less than 0.05) after training, whereas activities of Mg2+ -dependent ATPase and 5'nucleotidase did not change. In untrained dogs, exercise to the point of exhaustion elevated serum [K] from 4.4 +/- 0.5 to 6.0 +/- 1.0 meq/liter (P less than 0.05). In trained dogs, exhaustive exercise was associated with elevation of serum [K] from 3.8 +/- 0.3 to 4.2 +/- 0.4 (NS). The different response of serum [K] to exercise after training was not explainable by blood pH. Basal insulin levels rose from 7.0 +/- 0.7 microU/ml in the untrained dogs to 9.9 +/- 1.0 microU/ml (P less than 0.05) after training. Although insulin might have played a role in the acquired electrical hyperpolarization, the reduced exercise-produced hyperkalemia after training was not reversed by blockade of insulin release with somatostatin. Although the fundamental mechanisms underlying the cellular hyperpolarization were not resolved, our observations suggest that increased Na-K exchange across the sarcolemmal membrane, the increase of Na,K-ATPase activity and possibly increased electrogenicity of the sodium pump may all play a role in the changes induced by training.
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PMID:Muscle cell electrical hyperpolarization and reduced exercise hyperkalemia in physically conditioned dogs. 298 19

Around 1% of 8806 volunteers taking gossypol as a male contraceptive had hypokalaemic paralysis and more had simple hypokalaemia, the direct cause being renal potassium loss. In gossypol takers not showing hypokalaemia, serum potassium levels were within the normal range but were significantly lower than levels in controls. In the majority of patients suffering from gossypol-induced hypokalaemia, recovery was prompt and complete following potassium repletion, but in some men there were recurrent attacks of hypokalaemia during a period of several months to years after cessation of gossypol treatment. The incidence of hypokalaemic paralysis in gossypol takers showed distinct regional differences, being much higher in Nanjing, where the dietary potassium level of the inhabitants was low, than in Taian, where the dietary potassium level was high. In rats fed a low-K fodder, gossypol reduced the intracellular Mg and K concentrations of the skeletal muscle, while in regularly fed rats, this effect of gossypol was not observed. A potassium deficient diet could thus be considered a contributing factor in the development of gossypol-induced hypokalaemia. Potassium deficiency has also been shown to enhance the anti-spermatogenic effect of gossypol. Suggested mechanisms for the development of gossypol-induced hypokalaemia include inhibition of Na-K-ATPase activity, stimulation of prostaglandin biosynthesis, damage to the renal tubule, and modification of membrane transport.
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PMID:Gossypol-hypokalaemia interrelationships. 390 25

In order to examine the possibility that the changes in electrolytes in tissue alter the effect of thyroid hormone on NaK-ATPase, rats were fed either synthetic K-deficient diet or synthetic K-normal diet. K-deficient diet induced a reduction in K content in serum or kidney, while that of the liver remained unchanged. When a daily dose of 2.5 micrograms T3 was administered for 7 days to k-deficient rats, both Mg- and NaK-ATPase of the homogenate of liver and kidney were elevated, while the same dose failed to influence those enzymes in K-normal rats. Furthermore, T3 dose increased the Na content of liver and kidney in K-deficient rats, resulting in a significant decrease in th K/Na ratio in those tissue. Based on the estimation from chloride space, the decrease in K/Na was deemed to have occurred mainly in the intracellular space. As the levels of serum thyroid hormone and liver T3 were not influenced by K-deficiency, the effect of K depletion is likely to be mediated not through the alteration in thyroid hormone kinetics, but through some other mechanism such as the elevation of intracellular Na. The present study demonstrates that K deficiency may sensitize NaK-ATPase to the effect of thyroid hormone.
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PMID:Potassium deficiency enhances the effect of thyroid hormone on NaK-ATPase in liver and kidney. 610 7

Na-K-ATPase activity was determined in 10 segments of the rat nephron using a fluorometric microassay method [4]. The enzyme activity showed three peaks (greater than 200 pmol ADP min-1 mm-1) along the nephron of normal rats. These peaks were in the S1 portion of the proximal tubule, the medullary thick ascending limb from the inner stripe and the distal convoluted tubule. Feeding the rats a low potassium diet for 8 weeks produced a significant decrease in Na-K-ATPase activity in the cortical collecting duct, but no significant change in this enzyme in any other segment. The low potassium diet did not produce a significant change in Mg-ATPase in any nephron segments. We conclude that Na-K-ATPase activity along the rat nephron shows a pattern that is qualitatively similar to that seen in the rabbit nephron [4]. However, quantitatively the Na-K-ATPase activity in the rat nephron is greater than in the corresponding segments of the rabbit nephron. The results are consistent with the greater rate of glomerular filtration and Na+ reabsorption per rat nephron. Furthermore, our results suggest that the decrease in potassium excretion during potassium deficiency is modulated, at least in part, by the level of Na-K-ATPase activity in the cortical collecting duct.
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PMID:Effect of low potassium-diet on Na-K-ATPase in rat nephron segments. 628 58

Magnesium (Mg), a cofactor in numerous enzymatic reactions, is often ignored by clinicians, as the symptomatology of Mg depletion is not specific and usually associated with that of the cause of the depletion. Furthermore, the plasma Mg concentration (0.8 to 1.1 mmol.L-1) is only equivalent to one percent of the total body content. A Mg deficit may exist while plasma Mg concentration is normal. Therefore other techniques for Mg assessment, such as the repletion test, as well as red blood cell and lymphocyte concentrations have been used. A renewed interest for Mg occurred as numerous studies have shown the therapeutic efficiency of Mg and as the mechanisms of its haemodynamic effects have been recognized. Mg regulates Na-K-ATPase activity, K channels activity and, most of all, it is a natural calcium channel blocking agent. These properties explain its important place in electrophysiology of myocardial cells and the effects on the tension of smooth muscles, resulting in a vasodilation and a bronchodilation respectively. The antagonistic effect of Mg on calcium decreases the presynaptic release of acetylcholine at the neuromuscular junction and the release of epinephrine at the peripheral sympathetic nerves and the adrenals. Mg potentiates the effect of non-depolarizing muscle relaxants. A Mg deficiency occurs often in ICU patients, in alcoholics and during use of diuretics. Simultaneous administration of Mg is often required for treatment of potassium deficiency. Mg has an anti-arrhythmic effect towards digoxin-mediated dysrhythmias and torsades de pointes, and can be efficient in other arrhythmias. Systematic use of Mg seems to decrease mortality of acute myocardial infarction and is justified during cardiac surgery, often associated with hypomagnesemia, because of vasodilation of coronary arteries and in order to prevent occurrence of arrhythmias. Mg, because of its calcium channel blocking properties and as it lowers the release of epinephrine, is indicated for surgery of pheochromocytoma. In eclamptic and pre-eclamptic patients, the use of Mg is valuable, but not as an anti-epileptic agent. Other clinical uses of Mg have been proposed, but they are either anecdotal or of uncertain efficiency.
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PMID:[Indications for the use of magnesium in anesthesia and intensive care]. 857 7


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