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)

The association between arterial hypertension and obesity has been known for many years and demonstrated by epidemiological studies. The physiopathological mechanisms involved consist of increased extracellular volumes, hyperactivity of the sympathetic nervous system and the renin-angiotensin-aldosterone system, and abnormal ion exchanges between extra- and intracellular compartments. Recent studies have demonstrated an association between arterial hypertension and insulin resistance. Insulin resistance may well be the most important aetiological factor in this type of arterial hypertension as it stimulates both renal sodium reabsorption and sympathetic nervous system activity and reduces vascular Na-K-ATPase activity.
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PMID:[Arterial hypertension in patients with obesity. Role of hyperinsulinism and insulin resistance]. 209 34

In the presence of NADPH cytochrome P-450-dependent monooxygenases oxidize arachidonic acid giving rise to four epoxyeicosatrienoic acids (EETs) which are hydrolyzed enzymatically to dihydroxyeicosatrienoic acids (DHETs). EETs generate vasodilators. Allylic oxidation forms hydroxyeicosatetraenoic acids, of which 12(R)HETE is an inhibitor of Na(+)-K(+)-ATPase and renin release. Finally, omega and omega-1 hydroxylation of arachidonic acid generates 20- and 19-HETEs which are involved in the development of hypertension in SHR rats.
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PMID:Cytochrome P-450 metabolites of arachidonic acid: implications for blood pressure regulation. 212 86

To explore the etiology of altered Ca metabolism in essential hypertension, we studied parameters, i.e., maximal initial reaction velocity (Vmax) and Michaelis constant (Km), of Ca activation kinetics of Ca2(+)-ATPase in membrane fractions (isolated by a sucrose gradient) from platelets of blacks and whites, 27 of whom were essential hypertensives, 17 of whom were normotensives with a family history of essential hypertension, and 10 of whom were normotensives without a family history of the disease. The Vmax of hypertensives was significantly lower than in normotensives without a family history of essential hypertension (hypertensives, 14.99 +/- 1.71 nmol Pi.mg protein-1.min-1; normotensives, positive family history, 22.67 +/- 3.17 nmol Pi.mg protein-1.min-1; normotensives, negative family history, 27.54 +/- 4.37 nmol Pi.mg protein-1.min-1; overall, P = 0.0078). The Km was lower in both hypertensives and normotensives with a positive family history of essential hypertension as compared with normotensives with a negative family history of the disease (hypertensives, 1.70 +/- 0.23 microM; normotensives, positive family history, 1.38 +/- 0.2 microM; normotensives, negative family history, 2.79 +/- 0.58 microM; overall, P = 0.0251). Furthermore, the Km in whites was inversely related to plasma renin activity (r = 0.50; P less than 0.005). We propose that a lower Vmax for Ca2(+)-ATPase may play a role in the higher level of free Ca in platelets of essential hypertensives and that a higher affinity of the enzyme to Ca may reflect a process compensating for the lower Vmax. We also suggest that a higher Km for Ca2(+)-ATPase in juxtaglomerular cells of whites would result in blunting the release of renin.
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PMID:Kinetics of Ca2(+)-ATPase activation in platelet membranes of essential hypertensives and normotensives. 214 60

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

Normal pregnancy is associated with a poorly understood loss of vascular responsiveness to the pressor effects of infused angiotensin II. Since cellular cation metabolism appears to be a critical determinant of basal vascular tone and vascular reactivity, we have evaluated platelet ionized calcium, erythrocyte sodium, calcium and magnesium levels, and erythrocyte Ca-ATPase and Na/K ATPase activity in 15 normal black pregnant women (37.5 +/- 0.6 weeks gestation) and 10 normal age-matched nonpregnant black women. Plasma levels of factors potentially affecting vascular reactivity (endoxin, renin activity (PRA), and atrial natriuretic peptide (ANP] were measured by RIA and peripheral vascular resistance by biolectrical impedance. Peripheral vascular resistance was almost twice as high (P less than .003) in the normal group as in the pregnant women. Intracellular calcium concentrations were not significantly different in erythrocytes or platelets of the two groups. Although erythrocyte membrane Ca-ATPase was similar, Na/K ATPase activity was significantly higher in the pregnant subjects than in the nonpregnant controls, and intracellular sodium was lower. All three measured plasma factors, ANP, endoxin and PRA, were significantly elevated in the pregnant women. Our results suggest that the decrease in peripheral vascular resistance seen in normal pregnancy is probably not the result of alterations in cellular cation concentrations and/or cell membrane pump activity. However, the significant correlation between vascular reactivity and circulating ANP indicates this potent vasodilator may play a role in the observed decrease in peripheral vascular resistance associated with pregnancy.
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PMID:Effects of normal pregnancy on cellular cation metabolism and peripheral vascular resistance. 215 37

The present study was conducted in 15 essential hypertensives to evaluate the modifications of plasma levels of an endogenous Na/K ATPase inhibitor, blood pressure, forearm hemodynamics and plasma renin activity (PRA) elicited by an intravenous saline infusion (0.9% NaCl at the mean rate of 0.22 mL/min/kg body weight for 2 h). The response to saline was determined in the whole hypertensive population as well as in two subgroups of patients classified according to their rate of PRA suppression in response to volume expansion by comparison with normotensive controls (Normal- and Low-suppressors: N-S, L-S). Over the whole group of hypertensive patients, NaCl load provoked an increase in Na/K ATPase inhibitory activity, measured by enzyme-coupled assay, which was linearly related to PRA decline (r = 0.73) and to the increase in mean blood pressure (r = 0.57). These effects were clearly enhanced by considering L-S patients alone. Urinary Na/K ratio after saline infusion was significantly higher in L-S as result of a lesser potassium excretion in this subgroup. Our results support the hypothesis that acute volume expansion with saline causes an increase in plasma levels of an endogenous sodium pump inhibitor with hemodynamic effects and whose release is related to the individual handling of infused fluids and to the degree of renin-angiotensin-aldosterone suppression.
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PMID:Short-term plasma renin activity suppression by saline and release of a plasma endogenous Na/K ATPase inhibitor in essential hypertension. 215 4

Canrenone, a metabolic product of spironolactone, which competes with ouabain for binding to Na-K-ATPase at the digitalis receptor site and by itself inhibits Na-K-ATPase, was administered intramuscularly to reduced renal mass-saline drinking hypertensive and reduced renal mass-distilled water drinking normotensive rats for 8 days. Reduced renal mass-saline hypertension in the rat, is a low renin, volume expanded form of hypertension. Rats with this type of hypertension have been shown to have depressed arterial Na-K pump activity and increased Na-K pump inhibitory activity in their plasma. Canrenone treatment caused a progressive decrease in blood pressure in the hypertensive rats and this was associated with normalization of Na-K pump activity in arteries. Water and salt intake and excretion did not change. On the other hand, canrenone progressively increased blood pressure in the normotensive rats and this was associated with positive inotropy in isolated papillary muscles. These findings suggest that the depressed pump activity and the pump inhibitor play a role in reduced renal mass-saline hypertension in the rat and that the rise in blood pressure in the normotensive rats probably reflects canrenone's ability, by itself, to inhibit Na-K-ATPase.
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PMID:Effects of canrenone on blood pressure in rats with reduced renal mass. 215 66

There is evidence that three inhibitors of Na,K-ATPase activity--ouabain, K-free extracellular fluid, and vanadate--inhibit renin secretion by increasing Ca2+ concentration in juxtaglomerular cells, but in the case of vanadate, it is uncertain whether the increase in Ca2+ is due to a decrease in Ca2+ efflux (inhibition of Ca-ATPase activity, or inhibition of Na,K-ATPase activity, followed by an increase in intracellular Na+ and a decrease in Na-Ca exchange) or to an increase in Ca2+ influx through potential operated Ca channels (inhibition of electrogenic Na,K transport, followed by membrane depolarization and activation of Ca channels). In the present experiments, the rat renal cortical slice preparation was used to compare and contrast the effects of ouabain, of K-free fluid, and of vanadate on renin secretion, in the absence and presence of methoxyverapamil, a Ca channel blocker. Basal renin secretory rate averaged 7.7 +/- 0.3 GU/g/60 min, and secretory rate was reduced to nearly zero by 1 mM ouabain, by K-free fluid, by 0.5 mM vanadate, and by K-depolarization (increasing extracellular K+ to 60 mM). Although 0.5 microM methoxyverapamil completely blocked the inhibitory effect of K-depolarization, it failed to antagonize the inhibitory effects of ouabain, of K-free fluid, and of vanadate. A concentration of methoxyverapamil two hundred times higher (100 microM) completely blocked the inhibitory effects of vanadate, but still failed to antagonize the effects of ouabain and of K-free fluid. Collectively, these observations demonstrate that vanadate-induced inhibition of renin secretion cannot be attributed entirely to Na,K-ATPase inhibition, since in the presence of methoxyverapamil, the effect of vanadate differed from the effects of either ouabain (a specific Na,K-ATPase inhibitor) or K-free fluid. Moreover, it cannot be attributed entirely to a depolarization-induced influx of Ca2+ through potential-operated Ca channels, since methoxyverapamil antagonized K-depolarization-induced inhibition of renin secretion much more effectively than it antagonized vanadate-induced inhibition.
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PMID:Vanadate-induced inhibition of renin secretion is unrelated to inhibition Na,K-ATPase activity. 216 83

The ability of urine extracts to inhibit sodium and potassium-activated ATPase, cross-react with antidigoxin antibodies and induce natriuresis in rats was investigated in 10 healthy subjects, 10 cirrhotic patients without ascites (compensated cirrhotics), 27 nonazotemic cirrhotic patients with ascites and 10 cirrhotic patients with ascites and functional renal failure to assess whether reduced activity of natriuretic hormone contributes to sodium retention in cirrhosis. No significant differences were seen between healthy subjects and compensated cirrhotic patients in any of these parameters (sodium and potassium-activated ATPase inhibition = 178.5 +/- 19.8 vs. 247.4 +/- 48.7 nmol equivalent of ouabain/day; digoxinlike activity = 43.9 +/- 6.1 vs. 48.0 +/- 5.6 ng equivalent of digoxin/day; natriuretic activity = 0.36 +/- 0.15 vs. 0.63 +/- 0.27 mumol/min). Cirrhotic patients with ascites with and without functional renal failure showed significantly higher values of sodium and potassium-activated ATPase inhibition (708.1 +/- 94.0 and 529.2 +/- 53.9 nmol equivalent of ouabain/day, respectively), digoxinlike activity (136.9 +/- 7.2 and 116.3 +/- 7.9 ng equivalent of digoxin/day) and natriuretic activity (1.78 +/- 0.48 and 1.93 +/- 0.37 mumol/min) than healthy subjects and compensated cirrhotic patients. We saw no significant differences between these two groups of cirrhotic patients with ascites with respect to these parameters. In the cirrhotic patients studied, sodium and potassium-activated ATPase inhibition and antidigoxin antibodies directly correlated with the degree of impairment of hepatic and renal function, plasma renin activity and plasma levels of aldosterone and norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Natriuretic hormone activity in the urine of cirrhotic patients. 216 51

Racial differences in the regulation of Na+, K+, and Ca2+ have been shown both at the systemic and cellular levels. These include a higher incidence of "salt sensitivity," lower urinary K+ excretion, lower plasma renin activity, and higher circulating levels of immunoreactive parathyroid hormone and 1.25 dihydroxyvitamin D in blacks than in whites. Blacks exhibit a higher erythrocyte Na+ concentration, coupled with a lower maximal initial reaction velocity of erythrocyte Na,K-ATPase. Blacks also appear to differ from whites in erythrocyte Na+, K+ cotransport and Na-Li countertransport. Moreover, they show a higher activity of the Na(+)-H+ antiport in skin fibroblasts and a greater response of cellular Ca2+ signaling to agonists in serum. Mechanisms linking some of these racial differences in ionic metabolism to the increased propensity of blacks to develop essential hypertension are proposed, and the epidemiology and characteristics of this disease in blacks are reviewed.
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PMID:Essential hypertension in blacks: epidemiology, characteristics, and possible roles of racial differences in sodium, potassium, and calcium regulation. 217 6


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