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

Ouabain- and furosemide-dependent rate of sodium outflow through lymphocytes cellular membranes was measured in both healthy pregnant women and those with arterial blood hypertension caused by pregnancy. It was shown, that ouabain-dependent sodium outflow rate is decreased in healthy women in the I, II, and III trimester of pregnancy, while in women with arterial hypertension in the III trimester. No difference in sodium outflow rate both total and furosemide-dependent in healthy pregnant women during the I, II and III trimester, and in pregnant women with arterial hypertension due to pregnancy in the III trimester was noted. No difference in sodium outflow rate was noted in pregnant women with the arterial hypertension due to pregnancy with familial history of the hypertension.
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PMID:[Sodium outflow rate through lymphocyte cellular membranes in women with arterial hypertension caused by pregnancy and in health pregnant women]. 166 61

We studied the effects of ouabain and verapamil on endothelin-1(ET-1)-induced contraction of the mesenteric artery in prehypertensive spontaneously hypertensive rats (SHRs) and age-matched Wistar-Kyoto (WKY) rats. Rings of mesenteric artery of SHRs and WKY rats aged 4 weeks were superfused with physiological saline solution and isometric tension was measured. ET-1 (10(-9) or 10(-8) M)-induced contractions were significantly larger in WKY rats than in SHRs. ET-1 (10(-7) M)-induced contractions were not significantly different between SHRs and WKY rats. Verapamil markedly inhibited ET-1 (10(-7) M)-induced contractions both in SHRs and in WKY rats. Although the percent inhibition tended to be larger in SHRs than in WKY rats, the difference was not significant. Ouabain significantly increased ET-1 (10(-7) M)-induced contraction in the presence of verapamil both in SHRs and in WKY rats. The increase was significantly greater in SHRs than in WKY rats. As a result, ET-1 (10(-7) M)-induced contractions were significantly greater in SHRs than in WKY rats in the presence of verapamil and ouabain. These results suggest that in ET-1-induced arterial contraction, [Na+]i-mediated [Ca2+]i regulation such as the Na+/Ca2+ exchange system might be greater in SHRs than in WKY rats, and that this might be, at least in part, involved in the pathogenesis or maintenance of hypertension in SHRs.
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PMID:Effects of ouabain and verapamil on endothelin-1-induced contraction of mesenteric artery in young spontaneously hypertensive rats. 172 23

Mononuclear leucocytes were used as a cellular model for the in vitro measurements of volume, sodium and potassium content, sodium efflux rate constants and absolute sodium efflux in order to assess any cellular changes in young men at increased risk of developing essential hypertension, and to analyze whether any such changes were associated with borderline hypertension and/or heredity. Four groups of subjects were evaluated: 28 normotensive (NTO) and 20 borderline hypertensive (BHO) offspring of hypertensives, 12 borderline hypertensives with normotensive parents (BH) and 28 normotensive subjects with normotensive parents (NT). The cellular sodium/potassium contents of the four groups were not discernibly different. Ouabain insensitive sodium efflux rate constant and corresponding absolute efflux were significantly increased in offspring of hypertensives. Ouabain sensitive absolute sodium efflux was significantly increased in borderline hypertensives (BHO + BH) compared to normotensives (NT + NTO). These results indicate that leucocytes from subjects predisposed to hypertension possess an increased ouabain insensitive sodium transport mechanism and in subjects with borderline hypertension the sodium-potassium pump seems activated.
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PMID:Sodium content and sodium efflux of mononuclear leucocytes from young subjects at increased risk of developing essential hypertension. 232 32

Blood pressure response to chronic high salt intake and kinetics of red blood cell Na+ and K+ (Rb+) transport were studied in salt-sensitive (DS) and salt-resistant (DR) Dahl rats fed a high salt diet (8% NaCl) for 7 weeks from the fifth (young), 12th (adult), or 23rd (old) week of age. The kinetics of ouabain-sensitive Rb+ uptake and Na+ extrusion were determined in Na+ media as a function of both intracellular Na+ (Na+i, 2-8 mmol/l cells) and extracellular Rb+ (Rb+o). In addition, the kinetics of furosemide-sensitive Rb+ uptake (related to Rb+o) and the magnitude of the Na+ and Rb+ leaks were assessed. High salt induced hypertension in young and adult but not in old DS rats although red blood cell Na+ was slightly increased in all age groups of DS rats fed a high salt diet. The kinetic parameters of the Na(+)-K+ pump were similar in DS and DR rats fed a low salt diet. Ouabain-sensitive transport rates were not suppressed in erythrocytes of salt hypertensive Dahl rats. Maximal velocities of the Na(+)-K+ pump (related to Na+i) decreased significantly with age in all groups except in DS rats fed a high salt diet. This was compensated by an age-dependent increase in the affinity for Na+i so that no substantial differences in transport rates between young and old rats were seen at physiological cell Na+ and plasma K+ levels.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1990 Jun
PMID:Kinetics of Na+ and K+ transport in red blood cells of Dahl rats. Effects of age and salt. 234 24

To test whether leucocyte sodium pumps function abnormally in patients with essential hypertension specific tritium-ouabain binding (number of pumps) and ouabain sensitive uptake of rubidium-86 (86Rb+) (transport activity) were measured in mononuclear leucocytes from 37 untreated hypertensive patients and 85 normotensive subjects. Ouabain binding was lower and transport activity per binding site higher in the hypertensive patients before incubation (p less than 0.001), but both variables were normal after incubation for 72 hours with fetal calf serum. To determine whether a circulating inhibitor of sodium pumps was present in patients with hypertension ouabain binding and 86Rb+ uptake were measured in normal leucocytes before and after incubation for 72 hours with serum from 13 untreated hypertensive patients and 18 normotensive subjects. Ouabain binding was lower after incubation of cells with serum from hypertensive patients than after incubation with normal serum both before (p less than 0.01) and after (p less than 0.001) dialysis of the serum. The results suggest that in hypertension a circulating serum inhibitor of the sodium pump causes a chronic but reversible reduction in the number of pumps.
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PMID:Reversible inhibition of leucocyte sodium pumps by a circulating serum factor in essential hypertension. 242 43

Spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were used to investigate the adaptive biochemical changes in the myocardium in response to chronic afterload. Ouabain-inhibited Na+,K+-adenosine triphosphatase (ATPase) activity was decreased by 40% in myocardium of SHR compared with that from WKY, which may lead to increased intracellular Ca2+ through Na+-Ca2+ exchange. Similarly, alpha 1-adrenergic receptor density, estimated by [3H]prazosin binding, was decreased by 42% in myocardial membranes of SHR, while the affinity for the agonist and the antagonist was not altered. In contrast, the number of Ca2+ channels estimated by [3H]nitrendipine binding was increased by 45% in myocardial membranes of SHR, while the affinity was comparable between SHR and WKY. These differences between WKY and SHR in the membrane properties were not due to differential contamination of plasma membranes because the activities of other putative plasma membrane marker enzymes were comparable between WKY and SHR. There were no differences between WKY and SHR in the myosin ATPase activity estimated using myofibrils, actomyosin, and myosin. These results suggest that specific alterations have occurred in the plasma membrane properties of myocardium of SHR that result in altered intracellular Ca2+ metabolism. These alterations may have an important bearing on excitation-contraction coupling in myocardium of SHR.
Hypertension 1986 Jul
PMID:Alterations in the plasma membrane properties of the myocardium of spontaneously hypertensive rats. 242 36

The Na+-K+ pump activity was determined in femoral arterial smooth muscle from deoxycorticosterone acetate (DOCA)-salt hypertensive rats using potassium relaxation and ouabain-sensitive 86Rb uptake as indices. The membrane-stabilizing effect of calcium and its relation to Na+-K+ pump activity also were examined. Femoral arteries from DOCA-salt rats exhibited a greater relaxation in response to potassium addition after contraction with norepinephrine in a low potassium (0.6 mM) Krebs solution. The concentration of potassium required to produce a 50% relaxation was significantly less in DOCA-salt rats. Ouabain-sensitive 86Rb uptake was significantly greater at 3, 10, and 20 minutes of 86Rb incubation in femoral arteries from DOCA-salt rats. Linear regression analysis revealed a significant correlation between the uptake of 86Rb and time of incubation in both control and DOCA-salt rats. A significant difference in the slopes of the regression lines showed that the rate of uptake was greater in DOCA-salt rats. No difference was observed in ouabain-insensitive 86Rb uptake. A dose-dependent relaxation in response to increasing concentrations of calcium following contraction to norepinephrine was observed in femoral arteries from control and DOCA-salt rats. The relaxation was directly dependent on the level of extracellular potassium and was blocked by ouabain. Femoral arteries from DOCA-salt rats relaxed to a significantly greater extent in response to calcium at each level of potassium when compared with controls. These results provide further evidence for an increase in Na+-K+ pump activity in vascular smooth muscle from DOCA-salt hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1986 Nov
PMID:Sodium pump activity and calcium relaxation in vascular smooth muscle of deoxycorticosterone acetate-salt rats. 242 28

The goal of this study was to assess the role of the electrogenic Na+-K+ pump in controlling active tone in cremasteric arterioles of normotensive hamsters and hamsters with bilateral (two-kidney, two figure-8) Grollman hypertension. Arterioles of both groups exhibited a large transient dilation when the Na+-K+ pump was stimulated by superfusing the cremaster muscle with physiological salt solution containing 15 mM K+ after 20 minutes of 0 mM K+ superfusion. Arteriolar dilation in response to 15 mM K+ was significantly smaller in the hypertensive animals than in sham-operated controls. Ouabain (10(-5) M and 10(-3) M) inhibited arteriolar dilation in response to 15 mM K+ in both groups of animals. Resting diameters, total active tone (assessed by application of 10(-4) M adenosine), and arteriolar responses to inhibition of the Na+-K+ pump by superfusion with 0 mM K+ or ouabain were not significantly different in normotensive and hypertensive animals. These data indicate that an electrogenic Na+-K+ pump can regulate active tone in cremasteric arterioles, and that the maximum response of this pump to stimulation with 15 mM K+ is reduced in arterioles of hamsters with two-kidney Grollman hypertension.
Hypertension 1987 Jun
PMID:Reduced electrogenic sodium-potassium pump in arterioles during renovascular hypertension. 243 54

Primary aldosteronism is an uncommon cause of hypertension but one of particular interest because of its distinctive pathophysiological mechanism of blood pressure elevation. Aldosterone has been associated with increased Na+,K+-adenosine triphosphatase (ATPase) activity, but there is controversy over which sodium transport parameters are responsible for this increase. We measured intracellular sodium, ouabain-sensitive and ouabain-insensitive sodium efflux, and the number of Na+,K+-ATPase sites of washed erythrocytes, as well as Na+-Li+ countertransport and the Li+-K+ cotransport rate constant of lithium-loaded red blood cells (RBCs) in six patients with primary aldosteronism and in 50 normal subjects. Ouabain-sensitive sodium efflux was significantly (p less than 0.001) higher for the primary aldosteronism patients than for normal subjects (1.85 +/- 0.29 vs 1.51 +/- 0.21 mmol/L RBC/hr) even though the intracellular sodium concentration (7.2 +/- 1.5 vs 6.7 +/- 1.9 mM) and the number of the Na+,K+-ATPase sites per RBC (331 +/- 52 vs 385 +/- 97) were not increased. The elevated sodium efflux appeared to be due to a significant (p less than 0.001) increase in the rate constant (1.60 +/- 0.12 x 10(-15) vs 1.28 +/- 0.15 x 10(-15) mmol/site/hr) of the ouabain-sensitive sodium efflux. The rate constant decreased significantly (p less than 0.01) after treatment.
Hypertension 1988 Feb
PMID:Sodium transport parameters in erythrocytes of patients with primary aldosteronism. 244 94

The purpose of the present study was to examine the role of Na+,K+-ATPase activity in vascular adrenergic transmission of hypertension. In isolated perfused mesenteric vasculatures of spontaneously hypertensive rats (SHR, Okamoto and Aoki strain, seven- to ten-weeks-old) and age-matched Wistar Kyoto rats (WKY), the effects of ouabain, a potent Na+,K+-ATPase inhibitor, or partially purified plasma obtained from salt-induced hypertension on pressor responses and norepinephrine overflow were investigated. Pressor responses and norepinephrine overflow during electrical nerve stimulation were significantly greater in SHR than in WKY. Ouabain increased the stimulation-evoked pressor responses and norepinephrine overflow. This facilitation was more prominent in SHR than in WKY. Partially purified plasma obtained from reduced renal mass-salt hypertensive rats, which had a crossimmunoreactivity with digoxin, also increased the pressor responses and norepinephrine overflow during electrical nerve stimulation, and the effects were greater in SHR than in WKY. These results suggest that Na+,K+-ATPase on vascular adrenergic neurons has an important role in the regulation of neurotransmitter release, and that its activity might be enhanced in SHR.
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PMID:Facilitatory effects of ouabain and digitalis-like substance on adrenergic transmission in hypertension. 254 98


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