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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Ouabain-sensitive uptake of 86Rb, a measure of the Na+-K+ pump activity, was studied in tail arteries of rats made hypertensive with deoxycorticosterone and saline. 2. Decreased activity of the ouabain-sensitive Na+-K+ pump supports the hypothesis that the activity of Na+-K+ pump is suppressed in volume expanded hypertension.
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PMID:Altered activity of the sodium-potassium pump in arteries of rats with steroid hypertension. 21 75

The washout of radioisotopes was studied in aorta, femoral artery and portal mesenteric vein from controls and rats made hypertensive with injection of deoxycorticosterone (DOC) acetate. Experiments were also conducted on tonic (pulmonary artery) and phasic (portal mesenteric vein) smooth muscle from rabbits. The rate constants for the washout of 42K, 36Cl and 24Na from aorta were significantly elevated in the DOC hypertensives. Acute removal of extracellular K slowed the washout of 24Na by 50%, however, the rate constant for the DOC group remained higher than the controls. Increased turnover of 42K was also observed in the femoral artery and in a vessel (portal mesenteric vein) not exposed to the effects of high blood pressure in the rat. The rate constants for the washout of 42K, 36Cl and 24Na from phasic smooth muscle in rabbit were greater than the tonic type. Ouabain significantly slowed 24Na washout, however, the rate constant for the portal mesenteric vein remained higher than the pulmonary artery. DOC hypertension was associated with increased ion transport at several vascular sites. A similar change was observed for the phasic vascular smooth muscle from normal rabbits. A question is raised whether increased spontaneous activity of arteries reported to accompany DOC hypertension is the consequence of a membrane in transition from tonic to phasic behavior.
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PMID:Ion transport in tonic and phasic vascular smooth muscle and changes during deoxycorticosterone hypertension. 63 Jan 38

1. Several observations support the hypothesis that in rats of the Milan hypertensive strain elevated levels of a circulating ouabain-like factor might normalize the elevated Na+ reabsorption, but, on the other hand, might contribute to the development of hypertension. 2. As the receptor occupancy of this endogenous factor seems to be reversible, the aim of our study was to test, in vitro, the hypothesis of its presence in isolated kidneys from Milan hypertensive rats by studying the response to exogenous ouabain before and after prolonged washing. 3. The kidneys were isolated from adult Milan hypertensive rats and from age-matched normotensive controls and ouabain was given at two different experimental time intervals: shortly (15 min) after washout or after a further 60 min of washout (75 min in total). Comparative experiments with the diuretic hydrochlorothiazide were performed using the same protocol. 4. Ouabain given after 15 min of perfusion caused an increase in renal vascular resistance, diuresis and natriuresis; these haemodynamic and tubular responses were similar in kidneys from both Milan hypertensive and Milan normotensive rats. If given after the washout period, ouabain caused a comparable increase in renal vascular resistance, but a significantly greater natriuresis in kidneys from Milan hypertensive rats as compared with kidneys from Milan normotensive rats. On the other hand, hydrochlorothiazide caused similar natriuresis in kidneys from both strains after washout. 5. These results support the hypothesis that a factor, capable of interacting with the ouabain receptor on the Na+/K(+)-ATPase of tubular cells, is present in the kidney of adult Milan hypertensive rats and that it can be removed by prolonged washout.
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PMID:Differences in ouabain-induced natriuresis between isolated kidneys of Milan hypertensive and normotensive rats. 131 56

The present study investigated the role of ouabain-dependent inhibition of the Na(+)-K+ pump and stimulation of the brain renin-angiotensin system by looking at 1) the short-term and long-term effects of ouabain on arterial blood pressure, and 2) the acute and chronic effects of angiotensin II (ANG II) intraventricularly (i.c.v.) on the release of an endogenous inhibitor of the Na(+)-K+ pump. Ouabain infused subcutaneously in a dose of 1.5 mg.kg-1. 24 h-1 for 7 days did not affect arterial blood pressure in rats, whereas increases in both blood pressure and weight were observed in rats infused with ouabain at the same dose for a 4-week period. Plasma supernate obtained from pentobarbital-anesthetized dogs acutely treated with ANG II (1 microgram i.c.v. every 30 min for 2 h) induced a 44% decrease in the ouabain-sensitive 86Rb uptake by the rat tail artery which was prevented by pretreatment with saralasin i.c.v. Plasma supernate obtained from dogs that were infused for 4 days with ANG II (20 ng/min i.c.v.) and received saline as the drinking fluid also reduced by 34% the ouabain-sensitive 86Rb uptake by the rat tail artery. The present study provides evidence that chronic inhibition of the Na(+)-K+ pump for 4 weeks leads to the development of hypertension and that the release of an endogenous inhibitor of the Na(+)-K+ pump is implicated in the hypertension resulting from chronic stimulation of the brain angiotensin-system and an increase in sodium chloride intake.
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PMID:The ouabain-dependent Na(+)-K+ pump and the brain renin-angiotensin system. 131 74

Principally to ascertain whether mineral metabolism is involved in weight regulation, the 40 most obese of 1,774 children, aged 10-11 years, screened for obesity were compared with 46 age-matched controls. The obese children had more 3H-Ouabain erythrocyte binding sites (p = 0.04), higher intracellular sodium (p = 0.04), and lower plasma sodium (p = 0.002). After exclusion of the non-Scandinavians, the p values were p = 0.02, p = 0.03, and p = 0.03, respectively. Analysis of variance also showed the differences to be more dependent on obesity than on gender or nationality. It is concluded that obese children have more 3H-Ouabain erythrocyte binding sites indicating an increase of the sodium-potassium adenosine triphosphatase activity. The increase of intracellular sodium may increase the risk of future hypertension.
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PMID:Red cell sodium-potassium adenosine triphosphatase sites and intracellular sodium increased in obese school children. 132 34

Red blood cell Na+ content as well as ouabain-resistant Na+ and Rb+ (K+) transport (susceptible or resistant to inhibition by loop diuretics) were determined in spontaneously hypertensive rats (SHR) and normotensive Brown Norway (BN) rats the erythrocytes of which were incubated in either saline or Mg(2+)-sucrose medium. Elevated ouabain-resistant Na+ net uptake contrasted with slightly decreased red blood cell Na+ content in SHR compared with BN rats. Acceleration of furosemide- and bumetanide-sensitive Na+ fluxes contributed to enhanced ouabain-resistant Na+ influx into SHR erythrocytes in saline medium, whereas higher furosemide- or bumetanide-resistant Na+ efflux caused greater ouabain-resistant Na+ efflux in Mg(2+)-sucrose medium. Furosemide- and bumetanide-resistant Rb+ leaks were augmented in SHR erythrocytes. The association of the disclosed ion transport alterations with blood pressure was examined in 20 recombinant inbred strains derived from F2 SHR x BN hybrids. Ouabain-resistant Na+ uptake as well as furosemide- and bumetanide-resistant Na+ inward leaks (but not red blood cell Na+ content or furosemide- and bumetanide-sensitive Na+ net uptake) cosegregated with systolic and pulse pressures but not diastolic pressure of the recombinant inbred strains. In contrast, neither ouabain-resistant Na+ efflux nor any component of ouabain-resistant Rb+ uptake correlated positively with blood pressure of the recombinant inbred strains. Increased ouabain-resistant Na+ influx was compensated for by accelerated ouabain-sensitive Na+ extrusion because red blood cell Na+ content was not elevated in the hypertensive strains. Thus, high cell Na+ turnover rates might be related to genetic hypertension if an altered Na+ inward leak would be less effectively compensated for in tissues involved in cardiovascular regulation.
Hypertension 1992 Oct
PMID:Association of red blood cell sodium leak with blood pressure in recombinant inbred strains. 139 93

Ouabain has recently been reported to be an endogenous Na, K-ATPase inhibitor. To evaluate whether it exerts hypertensive action itself or amplifies the hypertensive action of small doses of mineralocorticoids, 5 mg deoxycorticosterone acetate (DOCA), 1 mg ouabain, or a combination of both were injected into mononephrectomized rats weekly for 6 weeks, and changes in blood pressure were evaluated. The blood pressures of control, DOCA-treated, ouabain-treated, and the combination treatment group at the sixth week were 138 +/- 3 (SE), 160 +/- 6, 144 +/- 6, and 201 +/- 14 mmHg, respectively. The blood pressure of rats given DOCA or ouabain alone was not significantly different from that of controls. In contrast, the blood pressure of rats given the combination of DOCA and ouabain was significantly higher than that of control rats and those given DOCA or ouabain separately. Cardionephromegaly and histopathological changes found in rats given the combination of DOCA and ouabain were consistent with the effects of an elevation of blood pressure. Further evaluation revealed that the amplification effect of ouabain on the hypertensive action of DOCA was dose dependent, with the minimum dose that caused the amplification effect being 0.25 mg/week. These results indicate that ouabain, although devoid of hypertensive action itself, amplifies the hypertensive action of small doses of DOCA and can cause a hypertensive state similar to that induced by larger doses of DOCA. It is inferred that the amplification effect of ouabain on mineralocorticoids is important in the genesis of hypertension.
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PMID:Ouabain as an amplifier of mineralocorticoid-induced hypertension. 144 41

Endogenous digital-like substance (DLS) is increased in patients with essential hypertension and is hypothesized to play a role in the pathogenesis of high blood pressure. Whether an increase in DLS in diabetic patients with hypertension is associated with a family history of hypertension or diabetic nephropathy was investigated. Plasma DLS was measured as Na(+)-K(+)-ATPase inhibitory activity (ATPI) in 100 Type 2 diabetic patients. Ouabain was used as a standard of Na-K-ATPase inhibition. Diabetic patients with hypertension demonstrated a greater ATPI level than normotensive diabetic patients (p less than 0.05). In patients with hypertension groups, the positive family history group had a higher ATPI level than the negative family history group (p less than 0.01). Microalbuminuria was not correlated with the ATPI level in diabetic patients. These results suggest that ATPI might play a role in the pathogenesis of hereditary hypertension associated with diabetes mellitus, but not have etiologic significance in diabetic nephropathy.
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PMID:Elevated endogenous digitalis-like substance in hypertensive diabetic patients with a family history of hypertension. 165 64

In the present study, we have examined the effects of ouabain on membrane fluidity of erythrocytes by use of an electron spin resonance (ESR) and spin-labeling method, and elucidated a possible role of Na+, K(+)-ATPase in the regulation of membrane fluidity in hypertension. Erythrocytes obtained from patients with essential hypertension were examined compared with those from age-matched normotensive subjects, and the ESR spectra for 5-nitroxy stearate incorporated into erythrocyte membranes were studied. The values of outer hyperfine splitting and order parameter (S) of the ESR spectra were significantly higher in patients with essential hypertension than in normotensive subjects. This finding shows that the membrane fluidity of erythrocytes might be lower in essential hypertension. Ouabain loading to erythrocytes decreased the membrane fluidity (S value was increased). The alternative degree was significantly greater in essential hypertension than in normotensive subjects. These results demonstrate that the membrane fluidity of erythrocytes might be highly dependent on the Na+, K(+)-ATPase activity in essential hypertension, which would suggest an abnormality in Na(+)-related cellular functions in hypertension.
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PMID:Effects of ouabain on membrane fluidity of erythrocytes in essential hypertension. An electron spin resonance study. 165 45

The activity of sodium-potassium pump was studied in mesenteric arteries and veins of rats, as well as its inhibition effect upon catecholamine-induced contractile responses and the time of relaxation of these vessels in normal rats and in those with DOCA-salt hypertension. The activity was measured by 86Rb [correction of 86Rh] up-take. A difference in the ouabain-sensitive take-up was found between arteries and veins. It was higher in normotensive rats' veins than in arteries; in hypertension, the activity of the pump tended to decrease in arteries and sharply increased in veins. Inhibition of the pump with ouabain reduced arteries' contractile responses to noradrenaline and phenylephrine in normotensive animals, whereas in hypertension the effect involved all the types of stimulation leaving intact the contractions of venous vessels. Ouabain increased the period of relaxation of arteries and veins in some types of stimulation in normal as well as in hypertensive rats.
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PMID:[The activity of the sodium-potassium pump of the mesenteric arteries and veins in normal rats and in DOCA-salt hypertension]. 166 90


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