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)

Many factors influence renal sodium excretion and blood pressure. We tested the independent effects of dietary calcium (Ca; 500 mg twice daily), potassium (KCl; 20 mEq three times daily), sodium-potassium dependent ATPase inhibition (digoxin), calcium channel blockade (nifedipine), and placebo, on acute natriuresis in 14 normal subjects while receiving 150 mEq/d sodium diets and 2 L normal saline intravenously over four hours. Each subject received each regimen in random sequence. Sodium balance before infusion was not different among the regimens. Plasma renin activity (PRA) was increased in subjects receiving nifedipine, while the plasma aldosterone concentration (PA) was not different among the regimens. None of the regimens influenced the clearance of inulin or paraaminohippurate (PAH) either before or after saline infusion. Only KCl and nifedipine affected sodium excretion compared to controls. KCl and nifedipine increased the amount of sodium excreted after the infusion was terminated. In the case of nifedipine, this natriuresis was sufficient to increase the 24-hour sodium excretion on that day to above that of the other regimens. The data support the notion that potassium and nifedipine may decrease blood pressure by facilitating sodium excretion. Nifedipine may also uncouple renin from aldosterone. Oral calcium supplementation and sodium-potassium dependent ATPase inhibition did not facilitate natriuresis.
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PMID:Effects of oral calcium, potassium, digoxin, and nifedipine on natriuresis in normal humans. 291 82

Interpopulation studies support the hypothesis of a causal relationship between sodium consumption and arterial hypertension. However, although this association has been contradicted by intrapopulation studies, the correlation between sodium and hypertension appears to be genetically determined, as there are both sodium-sensitive and sodium-resistant individuals. Sodium is essential for the maintenance of extracellular and plasma volume equilibrium. It is controlled metabolically by the interaction of several biological systems such as the renin-angiotensin-aldosterone system, the sympathetic nervous system and the kallikrein-kinin and prostaglandin systems. Thus, sodium has a definite role in the mechanism involved in the pathophysiology of the predominantly volume-dependent forms of arterial hypertension. Recently, different structural substances with natriuretic effects have been identified. Natriuretic hormone is a non-peptide substance which inhibits the Na,K-ATPase in response to extracellular volume increase. This hormone acts on the renal tubular cells reducing sodium reabsorption, and at an arteriolar level elevating peripheral resistance by increasing smooth muscle tension. Mammalian atria contain various precursors of biologically active peptides, with potent natriuretic and diuretic effects. They are released in response to volume loading and atrial stretch. Although some data suggest an important role for these natriuretic substances in fluid volume and blood pressure control, their place in physiology and in abnormal clinical states should be more definitively clarified in the next few years.
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PMID:Sodium and hypertension. Still a controversy in 1986. 294 88

Cardiopulmonary receptors influence renin release in a variety of physiological situations and in a fashion related to the degree of peripheral venous distensibility. We studied two groups of borderline hypertensives (BHTs) with different capacities to suppress plasma renin activity in response to saline infusion (0.20 mL/kg/per minute for 2 hours). Those BHTs with low suppressive capacity (L-supp) showed an increased venous distensibility in comparison with those with high suppressive capacity (H-supp). Saline infusion led to a significant increase in blood pressure only in L-supp BHTs, which was associated with enhanced 24-hour postloading natriuresis and raised plasma levels of an Na/K ATPase inhibitor (+12.2%). This result underlines the importance of venous distensibility as a determinant of pressor and humoral response to acute volume expansion.
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PMID:Importance of plasma renin activity suppression and venous distensibility on pressor and natriuretic responses to intravenous salt load in borderline hypertension. 296 4

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

Vascular (Na+,K+)-pump activity (ouabain-sensitive 86Rb+ uptake) and myocardial (Na+,K+)-ATPase activity are reduced in animals with various forms of low renin, experimental hypertension. On the other hand, vascular (Na+,K+)-pump activity is increased in Dahl salt-sensitive relative to resistant rats (a genetic model of hypertension), regardless of salt intake or blood pressure and it is also increased in Dahl salt-sensitive rats on high salt (8% NaCl) relative to low salt (0.4% NaCl) diets. It has been suggested that this increase in vascular (Na+,K+)-pump activity may be secondary to an increase in the vascular sarcolemmal permeability to Na+ in these salt-sensitive rats. In the present study, (Na+,K+)-ATPase activity of left ventricular microsomal fractions, was increased in Dahl salt-sensitive relative to resistant rats on low salt diets; however, this difference disappeared when these salt-sensitive and resistant rats were placed on high salt diets. In contrast, myocardial (Na+,K+)-ATPase activity was decreased in Dahl salt-sensitive rats on high relative to low salt diets. Evidence that this decrease in (Na+,K+)-ATPase activity is not secondary to myocardial hypertrophy in the hypertensive salt-sensitive rats, and mechanisms by which decreased cardiovascular (Na+,K+)-pump activity, increased sarcolemmal permeability or both, might contribute to elevated blood pressure, are discussed.
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PMID:Myocardial (Na+,K+)-ATPase activity in Dahl salt-sensitive and resistant rats. 298 28

A circulating Na+, K+-ATPase inhibitor may cause arterial hypertension in patients with suppressed plasma renin activity, either directly or by sensitizing peripheral vessels to alpha-adrenergic stimulation. This hypothesis was tested by evaluating forearm arteriolar (plethysmographic technique) response to exogenous alpha-adrenergic stimulation by a 2-minute intra-arterial infusion of norepinephrine (0.1 microgram/dl tissue per minute) and to Na+, K+-ATPase inhibition by sequential 20-minute intra-arterial infusions of ouabain (0.36 and 0.72 microgram/dl tissue per minute). Two groups of hypertensive subjects with suppressed plasma renin activity, either essential or secondary to aldosterone excess, were compared with age-matched and sex-matched hypertensive subjects with normal plasma renin activity (n = 7 per group). No significant differences in forearm vascular response to norepinephrine were found among the three groups. Ouabain caused a highly significant, dose-related increment in forearm vascular resistance that was not accompanied by changes in the contralateral limb or systemic blood pressure. No significant interindividual differences in vascular responsiveness to ouabain were found. The individual increments in forearm vascular resistance during ouabain administration were unrelated to basal values or to plasma aldosterone, norepinephrine, or potassium concentrations. These data are not consistent with the hypothesis that suppressed basal Na+, K+-ATPase activity is primarily a characteristic of hypertensive patients with unresponsive plasma renin activity. Overall, these results cast doubts on the possibility of linking the development of human low renin hypertension to an endogenous Na+, K+-ATPase inhibitor.
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PMID:Vascular responses to ouabain and norepinephrine in low and normal renin hypertension. 301 54

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

Congestive heart failure is a complex physiopathological state where both myocardial hypo-contraction and excessive peripheral vasoconstriction lead to lower cardiac output. The increase in cytosolic calcium concentration triggers the contractile processus. Digitalis inhibits the Na+/K+ ATPase enzyme and indirectly increases intracellular calcium concentration. beta 1 agonists increase the synthesis of cAMP-dependent protein kinase and hence the recruitment of new receptor-operated calcium channels which increase the calcium influx and the mobilization from its intracellular storage sites. Vascular smooth muscle contraction occurs with calcium influx into the cell resulting from various receptor activation. In congestive heart failure, activation of the sympathetic nervous system and of the renin-angiotensin system leads to neurohumoral-induced peripheral vasoconstriction. Renal effects of angiotensin II and aldosterone are responsible for sodium and water retention. alpha 1-blocking agents are drugs that block competitively the catecholamines effects on vascular receptors. Angiotensin I-converting-enzyme inhibitors block the formation of the key-element of the system: angiotensin II. Both alpha 1-blocking agents and converting-enzyme inhibitors show vasodilatator effects and acutely improve hemodynamic status of patients with congestive heart failure. Converting-enzyme inhibitors exhibit specific improvement of intrarenal hemodynamics and do not induced sodium and water retention in longterm therapy.
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PMID:[Pharmacological bases of the treatment of cardiac insufficiency]. 303 68

Calcium blockers of the dihydropyridine group may affect serum potassium level through an influence on the epinephrine mediated fall in serum K+. The effect of epinephrine infusion (12.5, 25 and 50 ng/kg/min) was assessed during placebo and after a 4-day treatment by nitrendipine in normal man. Nitrendipine treatment was associated with an enhancement in the fall of serum potassium induced by epinephrine. By contrast the response of arterial pressure, heart rate as well as the increase in blood glucose, plasma renin activity and the fall in plasma aldosterone and serum insulin levels induced by epinephrine were not affected by nitrendipine. Nitrendipine may potentiate the Na, K-ATPase stimulatory effect of epinephrine. Serum potassium should be carefully monitored in clinical situations associated with a consistent increase in circulating levels of epinephrine.
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PMID:[The hypokalemic effect of adrenaline is increased by nitrendipine in normal man]. 311 82

Potassium output from the body is regulated by renal excretion, which takes place predominantly in the late distal and cortical collecting tubules. The accepted model for potassium secretion implies the accumulation of potassium into the cell by the activity of basolateral Na-K-ATPase and its exit through voltage-dependent conductive channels. The factors regulating renal potassium secretion are potassium intake, distal urinary flow, systemic acid-base equilibrium, aldosterone, antidiuretic hormone and, probably, epinephrine. Renal handling of potassium is best studied by the response to the acute administration of furosemide. This loop diuretic not only increases sodium and chloride excretion but also enhances potassium and hydrogen ion excretion and stimulates the renin-aldosterone axis. The term "renal tubular hyperkalaemia" refers to a tubular dysfunction where the hyperkalaemia is disproportionate to any reduction in glomerular filtration rate (GFR) and not due primarily or solely to aldosterone deficiency or to drugs impairing either mineralocorticoid action or tubular transport. The syndromes of renal tubular hyperkalaemia mainly observed in childhood are "chloride shunt" syndrome, hyporeninaemic hypoaldosteronism and primary or secondary pseudohypoaldosteronism. Differential diagnosis between these conditions is easily made if attention is paid to the level of GFR, presence of sodium wasting, activity of the renin-aldosterone axis and renal response to acute administration of furosemide.
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PMID:Renal tubular hyperkalaemia in childhood. 315 64


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