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)

1. The effects of ouabain on renin secretion by rat renal cortical slices were studied. 2. Renin secretion was inhibited by 10(-3) M-ouabain in the presence of free Ca (10(-4) to 2.6 x 10(-3) M). Inhibition was blocked at Ca less than 10(-8) M. 3. The effect of free Ca on ouabain-inhibition was shown to be independent of the presence of EGTA, completely reversible, and unrelated to passive leakage of renin from non-viable cells, as assessed by simultaneous release of lactate dehydrogenase activity (LDH). 4. It is proposed that, as a result of inhibition of Na, K-ATPase by ouabain, (a) intracellular Na increases in the renin-secreting juxtaglomerular cells, (b) intracellular Ca increases, via an Na-Ca exchange mechanism, and (c) that Ca accumulation, in some unknown manner, inhibits renin secretion.
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PMID:Possible mechanism of the inhibitory effect of ouabain on renin secretion from rat renal cortical slices. 11 99

In the serum of two infant sisters with a congenital renal salt-losing syndrome, Na was rather low and K considerably increased. Even with Na levels of 126 mval/1, sodium was excreted in the urine. Creatinine and hippurate clearances were normal. Primary disturbances of the steroid metabolism were not detectable; plasma cortisol was normal, aldosterone and renin were compensatorily increased. Treatment with DOCA was unsuccessful. Whereas the first infant died (in another hospital), the second one throve well with high oral substitution of NaCl. There was no pathological findings other than a moderate hyperplasia of the juxtaglomerular apparatus, in a kidney biopsy. Except for minimal activity in the ascending limb of Henle's loop, there was no membrane bound Na, K-ATPase in the microdissected tubules. This finding most probably explains the renal salt loss, as this enzyme is necessary for the transcellular flow of sodium and potassium.
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PMID:Tubular Na, K-ATPase deficiency, the cause of the congenital renal salt-losing syndrome. 12 30

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

Defective potassium excretion with clinical acidosis, associated with fixed moderate sodium wasting, has been found to be a common abnormality in lead nephropathy. Lead poisoning has been shown by others to be associated with depression of the renin-aldosterone system and of sodium and potassium activated adenosinetriphosphatase (ATPase). Since these hormonal defects may contribute to the hyperkalemia and are reversible, lead poisoning should be treated aggressively. Management also requires proper regulation of dietary sodium, correction of acidosis, limitation of dietary potassium, and minimal use of antihypertensive agents, as well as the administration of allopurinal for urate control.
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PMID:Hyperkalemia and acidosis in lead nephropathy. 94 Oct 56

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

The effect of calcium antagonist nifedipine (N) was studied in the changes of blood pressure, total peripheral resistance, activity of the transport membrane ATPase of erythrocyte ghosts, the plasma level of digitalis-like factor and the plasma renin activity. The studies were performed in 10 healthy volunteers and in 19 hypertensive patients after the intake of a single dose of 20 mg N. The changes were studied in the hypertensives after the intake of the drug in daily doses of 3 times 10 mg over 4 weeks, too. The systolic and diastolic blood pressure and peripheral resistance of the forearm decreased in hypertensives after a single dose of nifedipine as well as after the treatment with 30 mg daily over 4 weeks (170.8/109.5 vs 145.3/98.3 mmHg). As compared with the membrane ATPase activity of normotensives, that of the hypertensives was distinctly depressed (0.403 vs 0.321 mumol P(i).mg-1.h-1; p less than 0.01), while after N treatment, the enzyme activity increased to values of those of the normotensives 0.403 mumol P(i).mg-1.h-1). The mean peripheral resistance was not significantly depressed after the long-term treatment with N (2,085 vs 1,535 dyn.s-1.cm-5), while in several hypertensives (9 of 19) a distinct reduction was measured. Analogous results were found in case of the mean renin activity and the activity of several hypertensives after the N treatment. The N effect on the membrane ATPase system is discussed in connection with the hypothesis of Blaustein [1977] (Na(+)- with consecutive Ca(2+)-overload of the cell) and a possible influence of the drug on the electrolyte transport via membrane.
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PMID:The reactivity of peripheral vessels of normo- and hypertensives. 131 13

To evaluate the antihypertensive and hormonal effects of oral magnesium supplementation, 17 inpatients with untreated, uncomplicated mild-to-moderate essential hypertension (EH) and 8 age-matched normotensive controls (controls) were given MgO orally 3 times a day at a daily dose of 1.0 g (0.6 g per day as Mg) for a period of 2 weeks. Supplementation of MgO elicited a significant fall in averaged mean blood pressure calculated with a 24-h ambulatory blood pressure monitoring system (MBP) in EH from a baseline value of 104.3 +/- 12.2 to 99.5 +/- 11.6 mmHg (p < 0.05), while controls remained unaltered from a baseline value of 85.1 +/- 11.5 to 84.5 +/- 13.3 mmHg. The percentage reductions in systolic and diastolic blood pressures were similar during daytime and nighttime in EH. According to the extent of reduction in MBP with magnesium supplementation, EH patients were divided into 2 groups, responder and nonresponder. The level of plasma renin activity (PRA) in the responder group was significantly higher than that of the nonresponder group (p < 0.05). After 2 weeks of magnesium supplementation, the plasma level of Na+, K(+)-ATPase inhibitory activity (PATPI), defined as equivalency to ouabain, was reduced significantly from 0.75 +/- 0.54 to 0.40 +/- 0.30 mumol ouabain/ml (p < 0.05) in the responder group, while it remained unaltered in controls and the nonresponder group. PRA, plasma aldosterone concentration, urinary epinephrine and norepinephrine excretion, and urinary sodium excretion did not change significantly in either control subjects or EH (responder and nonresponder groups). A significant negative correlation existed between the pretreatment PRA and changes in MBP after magnesium supplementation in EH (r = -0.65, p < 0.01), and there was a significant positive correlation between changes in PATPI and changes in MBP as a whole (r = 0.41, p < 0.05). These results support the view that oral magnesium supplementation is a useful approach to treatment of patients with uncomplicated essential hypertension, especially those with high plasmas renin activity. It appears that magnesium suppresses circulating Na+,K(+)-ATPase inhibitory activity to attenuate vascular tone, and thereby reduces blood pressure in EH.
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PMID:Effects of dietary magnesium supplementation on diurnal variations of blood pressure and plasma Na+, K(+)-ATPase activity in essential hypertension. 133 97

Cardiac glycosides in man inhibit renin secretion, probably through a direct effect at the renal level (i.e. inhibition of juxtaglomerular cell Na/K ATPase). Since there is evidence that the human adrenal possesses an intrinsic renin-angiotensin system, we investigated the effect of digoxin on the in vitro generation of renin and angiotensin II/III, as well as of aldosterone, by the human adrenal gland. Minced normal adrenal tissues were studied in a superfusion system, measuring in the 15-min superfusate fractions active renin by immunoradiometric assay and angiotensin II/III and aldosterone by radioimmunoassay, respectively. In a first set of four experiments using different concentrations of digoxin in sequence for 45 min periods, digoxin 10(-5), but not 10(-8) and 10(-6) mol/l, significantly reduced renin and angiotensin II/III output from adrenals, while no change in aldosterone was observed. In a second set of three experiments, the addition of digoxin 10(-5) mol/l for 120 min caused a sustained reduction of renin and angiotensin II/III, but not of aldosterone. In the final experiment, the decrease of renin and angiotensin II/III during superfusion with digoxin 10(-5) mol/l was significantly greater than that observed during superfusion with digoxin in the presence of antidigoxin antibodies. Our data indicate that digoxin at high doses reduces renin and angiotensin II/III but not aldosterone secretion by the human adrenal gland. This suggests two different effects of digoxin, probably both mediated by inhibition of the Na/K ATPase activity, on the adrenal renin-angiotensin- and aldosterone-secreting cells.
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PMID:Effect of digoxin on the in vitro secretion of renin and angiotensin II/III immunoreactivity by the human adrenal gland. 141 45

In addition to demonstrating evidences of increased sympathetic nervous system activity and marked left ventricular hypertrophy in salt-sensitive hypertensives, our group has also reported increased weight gain with salt overload in these patients. The increased weight gain suggests volume expansion, a situation already shown to increase plasma levels of a Na, K-ATPase inhibitor. Therefore, in the present study, digoxin-like factor (DLF) serum levels, spontaneous salt ingestion, nifedipine hypotensive effect, and plasma renin activity were evaluated in essential hypertensive subjects. Thirteen essential hypertensive outpatients were studied sequentially on an ad lib diet, a low salt diet (LSD = 30 mEq Na/day), and a high salt diet (HSD = LSD + 171 mmol/L NaCl/day), 1 week each. On the seventh day of LSD and HSD, DLF levels, mean blood pressure (MBP) response to nifedipine (10 mg sublingual), and plasma renin activity were measured. The MBP percent change from the seventh day of LSD to the seventh day of HSD (salt sensitivity) ranged from -13.7 to 20.9%. A positive correlation (r = 0.64, P < .01) was observed between salt sensitivity and 24-h urinary sodium excretion with an ad lib diet. The DLF serum levels correlated with the salt sensitivity both on LSD (r = 0.50, P < .05) and on HSD (r = 0.53, P < .05). Salt sensitivity was positively correlated with the difference of response to nifedipine between HSD and LSD (r = 0.78, P < .001). Plasma renin activity correlated inversely with DLF on LSD (r = -0.51, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Higher salt consumption, digoxin-like factor, and nifedipine response are associated with salt sensitivity in essential hypertension. 141 33


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