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)

Ouabain-sensitive ATPase activity (expressed as nmol ADP produced/h/mg (wet) nerve +/- SEM) was measured in homogenates of sciatic nerve from control rats and rats with streptozotocin-induced diabetes of 8 wk duration. Nerves from diabetic rats showed activity (21.7 +/- 2.0) which was significantly (p less than 0.05) less than that of controls (34.6 +/- 4.8). These animals also showed a deficit in conduction velocity (m/sec +/- SEM) of sciatic nerve motoneurones (50.7 +/- 0.4 vs. 57.7 +/- 0.7 in controls; p less than 0.001). In parallel, matched control and diabetic groups were treated daily with mixed gangliosides extracted from bovine brain (10 mg/kg i.p.). After such treatment for 8 wk the deficit in ouabain-sensitive ATPase activity did not develop in the diabetic group (treated diabetics, 31.9 +/- 3.7; treated controls, 34.5 +/- 3.8). However, the treatment did not affect the deficit in motor nerve conduction velocity (treated diabetics, 50.9 +/- 1.1 vs. treated controls, 57.9 +/- 0.5; p less than 0.001). Accumulations of the polyol pathway metabolites--sorbitol and fructose--together with depletion of nerve myo-inositol were similar in both diabetic groups. These data indicate an etiology for the conduction velocity deficit which differs from that of the deficit in ouabain-sensitive ATPase.
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PMID:Ganglioside treatment of diabetic rats; effects on nerve adenosine triphosphatase activity and motor nerve conduction velocity. 296 93

Idiopathic hypercalciuria is a common disorder whose inheritance suggests an enzyme abnormality in calcium transport. We measured calcium-magnesium-ATPase activity in erythrocytes from 38 patients (mean age [+/- SEM], 40 +/- 2.1 years) with idiopathic hypercalciuria (24-hour urinary calcium excretion greater than or equal to 0.1 mmol per kilogram of body weight) and a history of multiple calcium oxalate kidney stones. As compared with 41 healthy controls, the patients with hypercalciuria had increased erythrocyte-membrane calcium-magnesium-ATPase activity (64.2 +/- 2.19 vs. 51.6 +/- 1.91 nmol of ATP split per milligram per minute; P less than 0.01) and increased sodium-potassium pump activity (6866 +/- 233 vs. 6096 +/- 228 mumol of sodium per liter of red cells per hour; P less than 0.05). No significant difference between the two groups was found in erythrocyte sodium-potassium cotransport, sodium-lithium countertransport, or potassium content. In 66 patients with kidney stones (38 with hypercalciuria and 28 with normal calcium excretion), 24-hour urinary calcium excretion correlated with calcium-magnesium-ATPase activity (r = 0.46, P less than 0.001). Erythrocyte calcium-magnesium-ATPase activity remained unchanged in eight subjects studied after four months on a low-calcium diet. A study of 30 healthy families found significant correlations between mean values in parents and those in offspring for calcium-magnesium-ATPase (r = 0.68, P less than 0.001) and urinary calcium excretion (r = 0.45, P less than 0.02), with no significant correlations between parents with respect to these measures (r = 0.27 and r = 0.08, respectively). We conclude that abnormalities in erythrocyte calcium-magnesium-ATPase activity may represent an inherited defect in calcium transport related to the cause of idiopathic hypercalciuria.
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PMID:Abnormal red-cell calcium pump in patients with idiopathic hypercalciuria. 297 Nov 39

Material extracted and partially purified from plasma of the Sabra hypertension prone rats was found to be capable of 1) inhibiting the binding of 3H-ouabain to rat brain synaptosomes, 2) inhibiting the activity of rat brain microsomal Na, K activated adenosine triphosphatase, and 3) increasing the contractile force of rat heart muscle. The results demonstrate the presence of a ouabainlike compound in the plasma of these rats. The plasma concentration of this compound in Sabra hypertension prone rats was 698 +/- 199 nmol/ml in ouabain equivalents (SEM; n = 11) versus 2543 +/- 1140 nmol/ml (n = 9) in the Sabra normotensive strain. The presence of ouabainlike compound in the plasma is consistent with the hypothesis that this compound functions as a hormone that regulates Na, K activated adenosine triphosphatase activity and the physiological processes in which this enzyme is involved.
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PMID:Demonstration of a ouabainlike plasma compound in hypertension prone and hypertension resistant rats. 299 63

Hypoxia was induced by exposing rats to an atmosphere of 93% N2, 7% O2 for 4-48 hr. The animals became hypoxic as indicated by a decreased blood PaO2 (mean +/- SEM: 48 +/- 10 mm Hg). Hypoxia was accompanied by metabolic acidosis (pH 7.22 +/- 0.02) and decreased serum bicarbonate levels (9.0 +/- 4.0 meq/liter). Hypoxic rats also showed evidence of tissue hypoxia; liver tryptophan oxygenase levels were increased to 21 +/- 2 nmole/min/mg protein. In the hypoxic animals there was decreased jejunal mucosal (Na+-K+)-ATPase activity and an inhibition of active intestinal transport of sodium, glucose, 3-O-methylglucose, galactose, tyrosine, phenylalanine, and glycine as determined by in vivo perfusion studies. Jejunal fructose transport, which has a large passive component, was unaffected by hypoxia. The electrolyte, carbohydrate, and amino acid transport alterations produced by hypoxia were seen in the absence of an effect on jejunal cell number, DNA synthesis, or cell turnover. There was also no evidence of histological or ultrastructural damage. Furthermore, studies with a luminal macromolecular tracer, horseradish peroxidase, indicated that the jejunal lumen-to-blood barrier to macromolecules was also unaltered in these hypoxic animals. In vitro local oxygenation of the jejunum, by bubbling of 95% O2:5% CO2, markedly improved sodium and glucose (but not 3-O-methylglucose) absorption in hypoxic rats and control rats. The (Na+-K+)-ATPase activity of the jejunal mucosa of hypoxic rats was significantly enhanced by the local bubbling of 95% O2:5% CO2. Overall, our data indicate that during relatively mild conditions of hypoxia there is an inhibition of jejunal (Na+-K+)-ATPase activity and related transport processes that is prevented by in situ oxygenation.
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PMID:Alterations in jejunal transport and (Na+-K+)-ATPase in an experimental model of hypoxia in rats. 300 54

We measured the effects of ouabain on sodium-potassium ATPase (Na-K ATPase) specific activity (SA) and rubidium (Rb) transport in newborn (NB) and adult (Ad) sheep myocardium (myo), guinea pig myo and red blood cells (RBC), and human RBC. 50% inhibition of Na-K ATPase SA and Rb transport occurred at ouabain concentrations between 10(-4.8) and 10(-7.6) M in different species; within a species, 50% inhibition of Rb transport occurred at lower ouabain concentrations than 50% inhibition of Na-K ATPase SA. No differences between mature and immature tissues were found. Ouabain binding stability to Na-K ATPase extracted from myo and RBC did not vary with age. Binding studies revealed a KD X 10(-8) M of 0.87 +/- 0.09 for NB human RBC and 0.88 +/- 0.14 for Ad human RBC. Calculated RBC receptor density however, was higher in the Ad (1.25 +/- 0.08 sites/micron2) than in the NB (1.03 +/- 0.04 sites/micron2, p less than 0.01). Binding studies in extracted myocardial specimens showed a KD X 10(-8) M of 1.23 +/- 0.27 for NB and 1.09 +/- 0.46 for Ad; mM ouabain bound X 10(-12)/Na-K ATPase unit were 355 +/- 120 (SEM) for NB and 316 +/- 51 for Ad. These studies of cardiac glycosides reveal few age-related differences in drug binding or inhibition of monovalent cation transport.
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PMID:Effects of ouabain on monovalent cation transport in mammalian tissue. 300 50

Radioimmunoassays have been used to detect digoxin-like immunoreactive factors (DLF) in the plasma and urine of hypertensive patients and rats with deoxycorticosterone acetate (DOCA)-salt hypertension. Uninephrectomized rats (n = 9), given 15 mg DOCA . kg-1 . wk-1, were fed a standard rat chow supplemented with 2% NaCl (DOCA-HS); control animals (n = 15) were given vehicle injection and a specially formulated low-salt diet (0.05% NaCl). At 4 wk, DOCA-HS rats were hypertensive (121.4 +/- 10.1 vs. 88 +/- 4.4 Torr, mean +/- SEM, P less than 0.05) and excreted more DLF (2.7 +/- 1.1 vs. 0.2 +/- 0.1 ng digoxin equivalents . day-1, P less than 0.001) compared with control rats. DLF, partially purified from DOCA-HS urine by antidigoxin antibody immunoaffinity chromatography, was found to have a molecular weight less than 2,000, was resistant to acid hydrolysis or proteases, and had many properties of the cardiac glycosides, including inhibition of Na+-K+-ATPase activity, displacement of ouabain from human erythrocyte membranes, and inhibition of 86Rb influx into red blood cells. When DOCA-HS rats were switched to the low-sodium chow, DLF excretion dropped precipitously. No measurable DLF (less than 10 pg/ml) was detected in the plasma of rats eating either chow. However, greater than 95% of the urinary DLF could be attributed to a contaminant in the standard laboratory chow; rats fed the low-salt chow supplemented with 2% NaCl excreted much less DLF, and DLF was isolated from the standard chow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Excretion of artifactual endogenous digitalis-like factors. 301 5

A cytochemical assay has been developed to measure human plasma arginine vasopressin. It is based on the stimulation of Na+-K+, ATPase activity located in the outer medulla of the rat kidney, and is capable of detecting very low plasma arginine vasopressin concentrations, limit of detection 0.01 pmol/l. Specificity for vasopressin stimulation of the enzyme is conferred on the assay by the use of specific vasopressin antiserum. Index of precision of the assay is 0.21. Degradation of arginine vasopressin in plasma in inhibited by phenanthroline. Samples may be stored up to 8 weeks at -70 degrees C. Intra- and inter-assay coefficients of variation were 22% (n = 8) and 104% (n = 12), respectively. A sustained water load in eight healthy male adults caused a fall in plasma osmolality from a basal of 286.5 +/- 2.0 (mean +/- SEM) to 279.2 +/- 2.4 mmol/kg after the load (P less than 0.001), which was associated with a reduction in urine osmolality from 867 +/- 54 to 69 +/- 3 mmol/kg. Plasma immunoreactive arginine vasopressin fell from 1.3 +/- 0.3 pmol/l to become undetectable (less than 0.3 pmol/l), but plasma cytochemical arginine vasopressin decreased from 0.96 +/- 0.14 to 0.07 +/- 0.02 pmol/l. There was a curvilinear relationship between plasma osmolality and plasma cytochemical arginine vasopressin, which militated against the concept of an osmotic threshold for vasopressin release.
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PMID:Development of a cytochemical assay for plasma vasopressin: application to studies on water loading normal man. 301 8

Endogenous digitalis-like factors have been implicated in the adaptations that accompany renal insufficiency and in the pathogenesis of hypertension. We recently described several fractions of normal human plasma that inhibit NaK-ATPase and exhibit apparent digoxin-like immunoreactivity. To determine if hypertension and/or renal insufficiency affect plasma levels of these factors, we examined four patient groups: normotensive controls; hypertensive subjects with normal renal function; hypertensives with moderate renal insufficiency; and chronic dialysis patients. Plasma levels of digoxin-like immunoreactivity and NaK-ATPase inhibitory activity were significantly increased in hypertensive patients with mild renal failure (7.6 +/- 1.1 ouabain equivalents, mean +/- SEM, N = 21 vs 4.1 +/- 1.1 in normotensive controls, N = 20, P less than 0.05). NaK-ATPase inhibitory activity tended to be higher in patients with primary hypertension and normal renal function (5.5 +/- 0.7 ouabain equivalents, P less than 0.07); in dialysis patients, it was not different from controls. There was no correlation between NaK-ATPase inhibitory activity and blood pressure in any group. There was a significant rise in plasma NaK-ATPase inhibitory activity during dialysis (+ 1.8 +/- 0.7 ouabain equivalents, N = 22, P less than 0.03). As we have found that NaK-ATPase inhibitory activity in the plasma of normal humans can be separated into three distinct fractions, EI1, EI2, and EI3, we analyzed the plasma of 10 dialysis patients further. The increase in NaK-ATPase inhibitory activity could be attributed to fractions EI1 and EI3. These results suggest that plasma NaK-ATPase inhibitors increase with chronic renal insufficiency, but not hypertension alone. Although hemodialysis may acutely raise plasma levels, long-term dialysis returns them to the normal range.
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PMID:Endogenous digitalis-like factors in hypertension and chronic renal insufficiency. 302 36

Omeprazole (OME) is a novel acid secretion inhibitor, believed to act directly on the gastric proton pump, the (H+ + K+)-ATPase. Inhibition of ATPase activity is associated with an incorporation of [14C]OME into gastric vesicles containing the (H+ + K+)-ATPase, and both processes are greatly enhanced if the OME is exposed to acidic pH. This, and other evidence, suggests that the acidic environment of the (H+ + K+)-ATPase generates from OME a reactive intermediate which covalently inhibits the pump. We have compared the means by which the OME was acid-activated with the specificity of inhibition (amount of incorporation of omeprazole required to produce 100% inhibition of K+-stimulated ATPase activity). The stoichiometry of incorporation has been related to the number of detectable catalytic phosphorylation sites in each preparation (an index of the number of functional pumps). In lyophilised gastric vesicles, where the membrane barriers separating the cytoplasmic and luminal faces of the enzyme are substantially destroyed, incubation with OME at pH 6.1 produced a progressive inhibition and incorporation over 120 min. Complete inhibition of K+-ATPase required 13 +/- 3 (SEM; N = 4) moles of OME incorporation per phosphorylation site. In intact gastric vesicles, under conditions shown independently to result in proton pumping and the acidification of the vesicle interior (150 mM KCl, 9 microM valinomycin, 2 mM Mg-ATP pH 7.0), inhibition and incorporation occurred more rapidly (15 min). Complete inhibition of K+-ATPase required only 1.8 +/- 0.15 (SEM; N = 3) moles of OME per phosphorylation site.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The specificity of omeprazole as an (H+ + K+)-ATPase inhibitor depends upon the means of its activation. 302 28

Erythrocyte membrane Na+,K+-ATPase activity was measured using a bioluminescence technique in 28 hypertensive patients (24 with essential hypertension, 2 with renovascular hypertension and 2 with hypertension secondary to primary hyperaldosteronism) and in 28 normotensive control subjects matched for age and sex. Erythrocyte Na+,K+-ATPase activity was significantly reduced in the patients with essential hypertension (130.9 +/- 11.4 vs. 186.6 +/- 19.5 nmol ATP/mg prot per h; mean values +/- SEM; p less than 0.05) and in the patients with secondary hypertension. A significant negative correlation was found between erythrocyte Na+,K+-ATPase and systolic blood pressure (r = -0.603; p less than 0.01), but not between Na+,K+-ATPase and plasma renin activity or plasma aldosterone levels. These data confirm the findings of a number of previous studies reporting reduced activity of erythrocyte Na+,K+-ATPase possibly related to the presence of a circulatory inhibitor of sodium pump. The method, based on ATP assay by bioluminescence, presents a high degree of specificity as well as simple, rapid execution.
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PMID:Measurement by bioluminescence technique of erythrocyte membrane Na+,K+-ATPase activity in hypertensive patients. 303 52


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