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)

In normotensive humans with a positive family history of essential hypertension (FHH), blood pressure (BP) is often dysregulated. Resting BP already tends to be slightly higher than in age-matched control groups with negative FHH; BP responses to high sodium intake and perhaps to psychological and/or physical stress may also be exaggerated. Considering BP regulating factors, total exchangeable body sodium, whole blood volume, and their responses to low or high sodium intakes are normal in normotensive subjects with positive FHH; this does not exclude an existing although fully compensated regulatory disturbance. The response of plasma immunoreactive atrial natriuretic peptide levels to a high sodium intake seems to be impaired. On the other hand, a tendency for high ouabain-like Na+/K+-ATPase activity was reported in some normotensive subjects with positive FHH; data on central blood volume are lacking. Basal plasma renin, angiotensin II (AngII), and aldosterone levels, the reactivity of BP to acute increases in circulating AngII, and the responses of these variables to changes in sodium intake did not differe significantly between normotensive groups with a negative or positive FHH; this does not exclude a tendency for low renin-angiotensin activity in certain hypertension-prone families. The responsiveness of plasma aldosterone to acute rises in circulating AngII appeared to be largely unaltered when normotensive subjects with positive FHH were on moderate or high sodium intakes, but aldosterone responses may be blunted on a low sodium diet. Although a familial occurrence of subtle disturbances in AngII-dependent control of aldosterone and renal hemodynamics appears possible, BP regulation by the renin-angiotensin system is probably often intact at the stage of prehypertension. The finding of unaltered basal peripheral venous plasma norepinephrine (NE) and epinephrine levels and NE responses to changes in sodium intake, posture, or physical exercise in normotensive subjects with positive FHH has so far provided no evidence for enhanced sympathetic activity; nevertheless, direct analysis of regional nerve activity or NE release will be required to resolve this question. Regardless of the level of sympathetic activity, an exaggerated pressor responsiveness to NE occurs as a common disturbance in normotensive subjects with a positive FHH.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Dysregulation of blood pressure in normotensive offspring of hypertensive parents. 246 99

We tested the effect of dietary potassium (KCl, 20 mEq three times daily), calcium (Ca, 500 mg twice daily), sodium-potassium-dependent ATPase inhibition (digoxin), calcium channel blockade (nifedipine), and placebo on acute natriuresis in 14 normal subjects who received 2 L normal saline intravenously over 4 h. Plasma renin activity (PRA) was increased in subjects receiving nifedipine, while plasma aldosterone (PA) concentrations were not different among the regimens. 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 h sodium excretion on that day to above that of the other regimens.
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PMID:Facilitation of natriuresis with nifedipine in normal humans. 246 94

The Na,K-ATPase activity of erythrocyte membranes is markedly increased in normal-renin essential hypertensives. A temporal shift of the chronobiology of the erythrocyte-membrane-bound Na,K-ATPase in these patients is described. The disorder causes a loss of synchronism between the circadian rhythms of aldosterone and Na,K-ATPase. Such uncoupling phenomenon may explain the inversion of the day/night sodium excretion ratio and other disturbances of sodium metabolism found in essential hypertensives.
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PMID:Chronobiological evidence for an uncoupling of the Na,K-ATPase to aldosterone in normal renin hypertension. 254 13

1. Hypertension is a complication of autologous bone marrow transplantation when therapy includes multiple alkylating agents. We have sought to identify the factors underlying this hypertension. We measured weight, serum creatinine, plasma renin activity, aldosterone and digoxin-like immunoreactive factor (DLIF), by digoxin radioimmunoassay, in 18 patients. Plasma catecholamines were also measured in five patients. 2. Of the 18 patients studied, 15 became hypertensive. The variable most consistently associated with these individuals' hypertension was DLIF activity which was increased in 14 of the 15 hypertensive patients (P = 0.055, Fisher exact test). Serum creatinine was increased at some point in seven of the 15 hypertensive patients, weight was increased in five and plasma renin activity and aldosterone were increased in one. Catecholamines were not increased in any of the five patients in which they were measured. 3. The association between changes in mean arterial pressure (MAP) and changes in DLIF for the group as a whole was assessed by analysing one data pair per patient, representing the maximal MAP. This correlation was significant (r = 0.75, P = 0.001). 4. Within individual patients, changes in MAP and changes in serum DLIF concentrations were significantly correlated (r greater than 0.50, P less than 0.05) in six of 15 hypertensive patients. 5. Digitalis-like factor (DLF) was measured by inhibition of (Na+,K+)-adenosine 5'-triphosphatase in five patients and DLF and DLIF were significantly correlated (r = 0.081, P = 0.0001). DLF and MAP were also significantly correlated (r = 0.59, P = 0.002). 6. This represents the first longitudinal study of the relationship between DLIF and blood pressure in hypertensive individuals, and the results suggest that DLIF may contribute to the increased blood pressure in some of these subjects.
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PMID:Endogenous digoxin-like immunoreactive factor and digitalis-like factor associated with the hypertension of patients receiving multiple alkylating agents as part of autologous bone marrow transplantation. 255 6

The present study aimed to elucidate the role of Na, K-ATPase inhibitor in renal sodium metabolism in essential hypertension. Mean arterial pressure (MAP), heart rate(HR), urine volume (UV), urinary excretion of sodium (UNaV), endogenous creatinine clearance (Ccr), fractional excretion of sodium (FENa), plasma renin activity(PRA) plasma aldosterone concentration(PAC), plasma noradrenaline concentration (PNA) and urinary excretion of noradrenaline(UNA) were measured before and after intravenous injection of ouabain (0.1 mg/m2.BSA) in 12 normotensive(NT) and 22 mild-to-moderate essential hypertensive subjects(EHT). Following ouabain injection, UV, UNaV FENa significantly increased, but PRA decreased, in both NT and EHT. MAP, HR, Ccr, PNA, and UNA did not change significantly in either group. On the other hand, a significant decrease in PAC was observed in NT, but not in EHT. The changes of UNaV and FENa were significantly attenuated in EHT as compared to NT. No significant difference in change of MAP, HR, UV, Ccr, PNA, UNA, or PRA was demonstrated between NT and EHT. A significantly positive correlation was found between delta UNaV and delta FENa in both NT and EHT, while no significant correlation was observed between delta UNaV and delta MAP, delta UV, delta Ccr, delta PRA, delta PAC, delta PNA and delta UNA in either group. These results suggest that 1) Na, K-ATPase inhibitor clearly augments natriuresis by suppression of sodium reabsorption in renal tubules, 2) since this augmentation was attenuated, there is an elevation of endogenous Na, K-ATPase inhibitor(s) should be considered in EHT, and 3) an increase of the inhibitor might participate to the hypertensive mechanism in EHT.
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PMID:[The role of the Na, K-ATPase inhibitor in renal sodium handling in patients with essential hypertension]. 255 14

Na+-K+-ATPase activity and [3H]ouabain binding were studied in cardiac ventricles of single wrapped kidney and DOCA-NaCl hypertensive rats. It was found that the total Na+-K+-ATPase activity decreased in the DOCA-NaCl and kidney wrapped hypertensive rats. The decrease of enzyme activity in DOCA-NaCl hypertensive rats was due to extracellular fluid expansion induced by NaCl loading, as DOCA itself had no effect on the enzyme. All these alterations were specific for Na+-K+-ATPase, since Mg2+-ATPase and 5'-nucleotidase activities were unaffected. Binding studies with [3H]ouabain showed that the decrease in Na+-K+-ATPase activity was due to a reduction in the number of binding sites for ouabain rather than to a change of binding affinity. The reduced myocardial Na+-K+-ATPase activity observed in these two types of low renin hypertension, coupled with the observation of reduced vascular Na+ pump activity by others, suggests a common underlying defect in the cardiovascular Na+-K+ transport system of these hypertensive rats.
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PMID:Myocardial Na+-K+-ATPase activity and [3H]ouabain binding sites in hypertensive rats. 255 24

Red cell membrane Na(+)-K+ transport systems, renin-angiotensin-aldosterone system (RAAS) and atrial natriuretic factor (ANF) were studied in a group of 50 mild essential hypertensive patients (n = 25 for each group) age, sex and blood pressure matched. Na(+)-K+ ATPase and intracellular Na+ (Na+ i) were significantly different between the two groups (p less than 0.01). A slight difference was also seen for the Na(+)-K+ cotransport (p less than 0.05) as a likely consequence of the differences in the methodology of Na+ charge to study its efflux from the red cells in vitro. A negative correlation (r = -0.47, p less than 0.01) was observed between ANF and Na(+)-K+ cotransport suggesting an interrelationship of the two systems in the homeostasis in body fluid and electrolytes.
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PMID:[Erythrocyte cation transport in arterial hypertension: interrelation with the renin-angiotensin-aldosterone system and the atrial natriuretic factor]. 256 Sep 22

Concentrations of sodium-transport inhibitors (STI) which block the sodium-potassium-ATPase pump are increased in the plasma and urine of volume-expanded and low-renin hypertensive humans and animals. To evaluate the physiologic relevance of STI to blood-pressure-raising mechanisms, we have examined the in vitro properties of STI extracted from the urine of human subjects. STI produced a significant (by ANOVA: P less than .01) dose-contraction response in the isolated rabbit femoral artery. Moreover, small noncontractile doses of STI in this in vitro preparation produced a fivefold leftward shift in the contraction dose-response curve of norepinephrine (P less than .01) and a threefold shift for angiotensin II (P less than .01); at lower, physiologic, concentrations of these vasoconstrictor hormones the amplifications in contraction caused by STI ranged from 100% to 500%. In studies in calcium-free tissue bath solutions, the direct contractile action of STI was abolished; however, its amplification of responses to norepinephrine remained, suggesting that this latter effect of STI is not entirely dependent upon calcium influx into vascular smooth muscle cells. The glycoside ouabain produced effects identical to those of STI in arteries, but its actions on a rabbit atrium preparation were different: ouabain stimulated powerful inotropic effects, whereas human STI failed to cause myocardial contractions even though the amounts of STI administered had the same sodium-transport inhibitory capacity as the ouabain. Thus, the actions of human STI are primarily in the peripheral circulation, where they directly produce arterial contractions and also enhance contractile responses to other pressor hormones, suggesting that they may have a role in regulating systemic blood pressure.
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PMID:Effects of a human-derived sodium transport inhibitor on in vitro vascular reactivity. 280 70

Normal-renin essential mesor hypertensives are characterized by a consistent increase in erythrocyte membrane-bound Na/K-ATPase activity. Low-renin essential hypertensives exhibit, in contrast, a lower activity in Na/K-ATPase of cell membranes. This study documents a third disorder characterized by a temporal shift in the rhythmic activity of the erythrocyte membrane-bound Na/K-ATPase in normal-renin hypertensives. The disorder causes the synchronism with the aldosterone circadian rhythm to be invariably lost. The uncoupling phenomenon could be invoked to explain the inversion in the day-night sodium excretion rate found in essential hypertensives. In addition, it suggests that the circadian rhythm in Na/K-ATPase is under the control of cycling factors other than aldosterone.
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PMID:Internal desynchronization between circadian rhythms of plasma aldosterone and erythrocyte membrane-bound Na/K-ATPase. 281 94

We tested the hypothesis that a metabolic error may be the triggering mechanism which leads to blood-vessel hypertrophy and hypertension. Young spontaneously hypertensive rats (SHR) were fed a moderately high salt diet to exacerbate the purported metabolic error. Haematocrit values and rubidium transport were measured as evidence of renal ATP deficiency and blood-vessel adaptation. The renin system was inhibited in two groups of SHR by giving them enalapril to determine whether angiotensin II was involved in blood-vessel adaptation. Spontaneously hypertensive rats fed the moderately high salt diet had higher haematocrit values than normotensive rats fed the same diet or SHR fed Purina rat food, suggesting a renal ATP deficiency. Spontaneously hypertensive rats had higher Na+,K+-ATPase activity in thoracic aorta after 60 min incubation than a similar group given enalapril (P less than 0.001), suggesting blood-vessel adaptation. Possibly, angiotensin II within the vasa vasorum stimulates hypertrophy which, according to the Folkow hypothesis, leads to higher blood pressure, but may concomitantly increase the respiratory chain units which provide ATP for renal function and ion transport.
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PMID:Effect of a renin-system inhibitor on blood-vessel adaptation in spontaneously hypertensive rats. 282 Dec 7


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