Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phenytoin stimulated renin secretion from rat renal cortical slices. A sigmoid relationship was found between stimulatory effect and log concentration, from 1 to 8 mg/100 ml. The ED5C was 2.8 mg/100 ml. Basal secretion and the stimulation of secretion elicited by phenytoin were blocked by incubating slices in a K-free medium and by adding 1 mM ouabain to the medium (both of which inhibit Na,K-adenosine triphosphatase activity and increase intracellular Na concentration), and by reductions in the Na concentration of the incubation medium. NaCl in the incubation medium was replaced by choline chloride so that osmolality and Cl concentration were held constant. It is suggested that renin secretion rate is directly related to the transmembrane Na gradient, that phenytoin stimulates secretion by increasing the gradient, and that ouabain, K-free medium and reductions in Na concentration of the medium inhibit secretion by reducing the gradient.
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PMID:Phenytoin stimulates renin secretion from rat kidney slices. 51 21

Renal functional abnormalities constituting the syndrome of postobstructive diuresis imply both altered tubular and glomerular membrane properties. To determine the morphologic and ultrastructural correlates of this disorder a rat model was developed and 32 postobstructed kidneys were studied by light and electron microscopy at the midpoint of diuresis and compared to 22 controls. The abnormal morphology was: dilated distal tubules and collecting ducts, isolated proximal and distal tubule cells that allowed free access of luminal contents to the basement membrane, widened terminal bars and intercellular spaces, thickening of the glomerular basement membrane and, depending upon the portion of nephron, normal or reduced adenosine triphosphatase and acid phosphatase content. In order to confirm the functional nature of the nephrons studied as well as to assess glomerular and tubular permeability, horseradish peroxidase and cytochrome c were infused. These tracers, normally permeable to the glomerular basement membrane, were found in the intercellular spaces and to a lesser extent within cell organelles in the postobstructed diuretic animals whereas controls demonstrated a retarded filtration of horseradish peroxidase, no tracer in the intercellular spaces and large amounts of tracer contained within cell organelles. Absence of enzyme activity in the medulla and reduced dark to light cell ratios in the cortical collecting ducts correlated with prior observations made by others of diminished concentration and acidification processes, respectively. An increase in adenosine triphosphatase activity and renin granules within the juxtaglomerular cells indicated increased renin activity. These observations suggest that the renal functional abnormalities of postobstructive diuresis are attributable to altered glomerular and tubular permeabilities as well as with changes in metabolic activity.
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PMID:A histochemical and morphologic study of postobstructive diuresis in the rat. 99 66

To elucidate the mechanism of hyperkalemia in diabetic patients without renal failure, we investigated (Na(+)-K+) adenosine triphosphatase (ATPase) activity in erythrocyte membrane, erythrocyte Na+ and K+ content, and plasma endogenous digitalis-like substance in control subjects (n = 16) and non-insulin-dependent diabetes mellitus (NIDDM) patients (n = 62). NIDDM patients were divided into normokalemic patients (NKDM, n = 48) and hyperkalemic patients (HKDM, n = 14). There was no difference in plasma glucose or hemoglobin A1c (HbA1c) levels, plasma renin activity (PRA), and plasma aldosterone concentrations (PAC) between NKDM and HKDM patients. (Na(+)-K+)ATPase activities in NIDDM patients were significantly reduced compared with those in control subjects (0.336 +/- 0.016 mumol-inorganic phosphate [Pi]/mg protein/h, mean +/- SEM, P less than .05), and (Na(+)-K+)ATPase activities in HKDM patients (0.243 +/- 0.015 mumol Pi/mg protein/h) were significantly reduced compared with those in NKDM patients (0.295 +/- 0.008 mumol Pi/mg protein/h, P less than .01). Plasma K+ content had a significant negative correlation with (Na(+)-K+)ATPase activity in diabetic patients (r = -.365, P less than .01). Erythrocyte Na+ content had a significant negative correlation with (Na(+)-K+)ATPase activity in control subjects (r = -.619, P less than .05). There was no difference in plasma endogenous digitalis-like substance among the three groups. (Na(+)-K+)ATPase activity was not significantly correlated with plasma endogenous digitalis-like substance in control subjects and diabetic patients. These findings suggest that the reduction of (Na(+)-K+)ATPase activity, which was not related to plasma digitalis-like substance, may be partly responsible for hyperkalemia in diabetic patients.
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PMID:Reduction of erythrocyte (Na(+)-K+) ATPase activities in non-insulin-dependent diabetic patients with hyperkalemia. 131 28

An increased venous tone responsible for changes in systemic hemodynamics has been described in borderline hypertensive patients along with the release, in response to intravenous sodium chloride, of an endogenous sodium ion/potassium ion adenosine triphosphatase (Na+/K+ ATPase) inhibitor with vasoconstrictive properties. The hemodynamic and humoral effects of a 2-hour intravenous saline infusion were studied in 25 borderline hypertensives characterized on the basis of their forearm venous distensibility (VV30) in normal (n = 15) and low (n = 10) VV30. VV30 was slightly reduced by saline in the entire hypertensive group (1.47 vs 1.36 ml/100 ml; p less than 0.05), whereas blood pressure and plasma Na+/K+ ATPase inhibitor were unchanged. Normal VV30 showed a sudden increase in plasma Na+/K+ ATPase inhibitor in response to saline associated with an increase in blood pressure, a forearm arterial and venous constriction, and a sluggish suppression in plasma renin activity, whereas low VV30 exhibited a completely opposite pattern. The changes in plasma Na+/K+ ATPase inhibitor inversely correlated to VV30 decreases in borderline hypertensives with normal VV30 (r = -0.49; p less than 0.05), whereas they did not in all hypertensive patients. Atrial natriuretic peptide response to saline infusion was delayed in normal VV30 and inversely related to the changes in Na/K+ ATPase inhibitory activity (r = -42; p less than 0.05) attained after 2 hours of infusion in the entire hypertensive population. Results of this study suggest the ability of acute volume expansion to reduce peripheral venous distensibility in borderline hypertensive patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pattern of peripheral venous response to volume expansion in borderline systemic hypertension. 214 96

Congestive heart failure is characterized by both disturbances in electrolyte homeostasis and neuro-hormonal regulation. Total body potassium is reduced, and this reduction bears a modest relation to activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. Patients with decompensated heart failure show increases in both plasma epinephrine and plasma norepinephrine, whereas patients with chronic stable heart failure usually have an increase only in plasma norepinephrine. High levels of circulating epinephrine may contribute to the development of hypokalemia by activating skeletal muscle and liver membrane beta 2-adrenergic receptors, which in turn stimulate intracellular cyclic adenosine monophosphate to activate the membrane-bound Na+K(+)-adenosine triphosphatase pump. The net result is that potassium flux across the cell membrane from the extracellular to the intracellular space increases, setting the stage for hypokalemia and possibly serious ventricular arrhythmias. Other mechanisms that may contribute to the development of hypokalemia in heart failure include the kaliuresis brought on by excessive levels of aldosterone. Moreover, it is likely that the activity of facilitated by concomitant activation of the renin-angiotensin system. Increased sympathetic nerve activity may then release additional renin from the kidney (by way of a beta 2-adrenergic mechanism). Therefore, both the sympathetic nervous system and the adrenal medulla may interact to cause hypokalemia in patients with heart failure. Because hypokalemia is known to predispose patients to ventricular arrhythmias, it may be prudent to aggressively maintain serum potassium levels in patients with heart failure in the range of 4 to 5 mEq/liter.
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PMID:Interaction of the sympathetic nervous system and electrolytes in congestive heart failure. 230 25

Our earlier studies of cataracts in Dahl salt-sensitive (DS) rats suggested the possibility of altered lens ion transport as a contributing factor in cataractogenesis in this genetic model. We also observed that those weanling DS rats with the greatest pressor response to a high salt diet eventually developed cataracts, and that changes in salt intake modified cataract formation. In the present studies, we measured lens 86Rb uptake as an index of sodium-potassium adenosine triphosphatase [(Na+,K+)-ATPase] activity in weanling DS rats before the development of cataracts or sustained hypertension. Additionally, plasma renin activity was measured to indirectly assess our hypothesis that the difference between cataract-prone DS rats and DS rats unlikely to develop cataracts might be a difference in degree of salt sensitivity. At the age of 4 weeks, 50 DS and 25 salt-resistant (DR) rats were given a high sodium diet for 2 weeks, at which time the rats were divided into three groups based on the systolic blood pressure response, that is, cataract-prone DS rats with systolic blood pressure equal to or greater than 155 mm Hg, DS rats unlikely to develop cataracts with systolic blood pressure less than or equal to 125 mm Hg, and DR rats. Lens and aqueous humor Na+ and K+, lens dry weight, and water content were not significantly different among the three groups of weanling rats. Plasma renin activity was lowest in cataract-prone DS rats and low in DS rats unlikely to develop cataracts when compared with values in DR rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lenticular rubidium uptake and plasma renin activity in weanling cataract-prone salt-sensitive rats. 240 57

1. To test the hypothesis that NaCl increases blood pressure, while NaHCO3 does not, we measured the effect of an NaHCO3-containing mineral water on blood pressure in stroke-prone spontaneously hypertensive (SHR-SP) and Wistar-Kyoto (WKY) rats. We compared mineral water with equimolar amounts of NaCl and demineralized drinking water in six groups of 20 rats each over 24 weeks. 2. NaCl consistently increased blood pressure in both SHR-SP and WKY compared with demineralized water, while mineral water did not. 3. We studied the possible role of sodium-regulating hormones. Sodium, potassium-dependent adenosine triphosphatase activity was decreased by NaCl and by age, but not by mineral water. The concentration of atrial natriuretic peptide was greater in SHR-SP, but was not influenced by the two regimens. Components of the renin-angiotensin-aldosterone system and 18-hydroxydeoxycorticosterone tended to decrease with NaCl, but not with mineral water. 4. Plasma pH values in the six groups of rats were not different; however, SHR-SP had consistently lower PCO2 and HCO3- values and higher anion gap values than WKY rats. These values were not influence by the two regimens. 5. NaCl elevates blood pressure in SHR-SP while NaHCO3 does not. The changes in hormones regulating sodium homoeostasis suggest that NaCl induces volume expansion while NaHCO3 does not. The effect may be related to influences on renal sodium reabsorption by chloride and bicarbonate. The possible role of increased proton excretory activity in SHR-SP remains to be determined.
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PMID:Effect of sodium chloride and sodium bicarbonate on blood pressure in stroke-prone spontaneously hypertensive rats. 284 Feb 35

1. We measured ouabain-insensitive adenosine triphosphatase (ATPase), sodium, potassium-dependent adenosine triphosphatase (Na+,K+-ATPase) and intracellular Na+ and K+ in the erythrocytes of 19 healthy volunteers, before and after supplementation of their normal diet was 6.0-8.9 g of salt (102-137 mmol of NaCl) per day, for 5 days. 2. The subjects had a small but significant gain in weight. Mean plasma renin activity decreased from 1.57 to 0.73 pmol of angiotensin 1 h-1 ml-1 and plasma aldosterone from 0.46 to 0.24 nmol/l. 3. Total ATPase activity fell from 197.9 nmol of inorganic phosphate h-1 mg-1 during the control period to 173.5 during the high-salt period (P less than 0.0125). Na+, K+-ATPase activity fell from 162.2 to 141.4 nmol of inorganic phosphate h-1 mg-1 (P less than 0.05). Intracellular Na+ and intracellular K+ did not change. 4. These results are consistent with the hypothesis that salt-induced volume expansion causes the release of a factor inhibitory to the Na+ pump.
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PMID:Effect of high salt intake on sodium, potassium-dependent adenosine triphosphatase activity in the erythrocytes of normotensive men. 284 5

Previous results have demonstrated that two inhibitors of Na-and-K-activated adenosine triphosphatase (ouabain, vanadate) lead to stimulated prostaglandin E2 release and to inhibited renin secretion in the rat renal cortical slice preparation. It was speculated that stimulation of phospholipase A2 activity accounted for the effect on prostaglandin E2 release. We used the same preparation in the present experiments, and showed that another inhibitor of Na-and-K-activated adenosine triphosphatase (K-free incubation medium) stimulates prostaglandin E2 release and inhibits renin secretion. Quinacrine antagonized the stimulatory effects of ouabain, vanadate, and K-free medium on prostaglandin E2 release (consistent with phospholipase A2 involvement), but did not antagonize their inhibitory effects on renin secretion. Collectively, these observations lend further weight to the argument against a mediatory role of prostaglandin synthesis in the renin secretory process.
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PMID:Quinacrine antagonizes the effects of Na,K-ATPase inhibitors on renal prostaglandin E2 release but not their effects on renin secretion. 298 87

We have examined cardiovascular pressor responsiveness to infused norepinephrine (NE) as related to endogenous plasma NE and plasma renin and to platelet free cytosolic (Ca2+) in 36 patients with early-stage kidney disease and 27 matched normal subjects. The 27 hypertensive patients and the normal subjects did not differ in blood volume, plasma renin, and NE; however, the hypertensive patients had a higher exchangeable body sodium content. Basal plasma NE levels, the relationship between plasma NE measured during NE infusion and the corresponding NE infusion rate, as well as the total plasma clearance for NE did also not differ significantly between the two study groups. In contrast, the threshold or pressor doses of infused NE significantly decreased in the patients with kidney disease. Antihypertensive pharmacotherapy with (Ca2+) channel blockers and/or loop diuretics normalized blood pressure and cardiovascular NE hyperresponsiveness and reduced blood volume, exchangeable body sodium, and platelet free cytosolic (Ca2+). In contrast, experimental digitalisation as a model for in vivo sodium/potassium adenosine triphosphatase inhibition augmented NE responsiveness and raised platelet free cytosolic (Ca2+). Incubation of platelets from normal subjects with plasma ultrafiltrate from hypertensive patients gave evidence for an endogenous factor capable to raise free cytosolic (Ca2+) and to act synergistically with digoxin. Hypertension secondary to early-stage kidney disease is related to an impairment of sodium excretion leading to an expansion of blood volume and exchangeable body sodium. This may result in increased secretion of endogenous factors, leading to alterations of cytosolic (Ca2+) homeostasis of vascular smooth muscle cells followed by elevated peripheral resistance and thus blood pressure.
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PMID:Hypertension secondary to early-stage kidney disease: the pathogenetic role of altered cytosolic calcium (Ca2+) homeostasis of vascular smooth muscle cells. 849 19


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