Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ouabain-sensitive Na+-K+-ATPase activity in red cell membranes, kidney cortical tissue, myocardium and adrenal glomerulosa tissue was examined in SHR and WKY rats at 6, 9, and 12 weeks of age. Red cell membrane enzyme activity was decreased (p less than 0.001) at 9 and 12 weeks of age in SHR. This activity was negatively correlated (r = -0.69, p less than .005) with blood pressure at 9 and 12 weeks. Kidney cortical enzyme activity was also decreased (p less than 0.001) in the SHR at 9 and 12 weeks of age. This decreased kidney enzyme activity was also inversely related to 9 and 12 week blood pressures (r = -0.71, p less than 0.001), urinary Na excretion (r = -0.62, p less than .005), and urinary Ca and K excretion. Myocardial enzyme activity was not decreased until 12 weeks in the SHR, and adrenal glomerulosa activity was not different in the SHR and WKY at any of the three ages that this enzyme was measured. Of the tissues examined decreased Na+-K+-ATPase activity in the erythrocyte membrane and in kidney cortical tissue appears to coincide best with the development of hypertension in the SHR. This study lends further support to the concept that alterations in membrane cation transport may be an important factor in the development of high blood pressure in SHR.
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PMID:Reduced sodium-potassium dependent ATPase and its possible role in the development of hypertension in spontaneously hypertensive rats. 629 28

Various parameters of erythrocyte membrane sodium transport were measured in patients with untreated essential hypertension, in the normotensive offspring of parents with hypertension, and in patients whose hypertension had been controlled by medication. Net sodium efflux, measured by an isotopic tracer technique, was 2.12 +/- 0.17 mM Na+/1 of red blood cells (RBCs)/hr in patients with untreated essential hypertension, compared with 1.55 +/- 0.12 mM Na/1 of RBCs/hr in a group of normotensive controls (p less than .025). Partitioning sodium efflux into ouabain-sensitive and ouabain-insensitive components revealed a significant elevation of both components of membrane sodium transport in the patients with untreated essential hypertension. Ouabain-sensitive sodium efflux was 1.38 +/- 0.09 mM Na/1 RBCs/hr in the patients, compared with 1.04 +/- 0.07 mM Na/1 RBCs/hr in the controls. Ouabain-insensitive sodium efflux was also increased from 0.51 +/- 0.05 mM Na/1 RBCs/hr in the controls to 0.74 +/- 0.09 mM Na/1 RBCs/hr in those with untreated hypertension. Despite these changes in sodium efflux, Na,K-ATPase activity in the erythrocyte membrane, measured at maximum velocity (Vmax), was normal, suggesting that the observed abnormalities in membrane sodium transport in patients with untreated essential hypertension resulted from a change in pump control mechanisms rather than a change in enzyme activity. With the techniques used in this study we were unable to identify changes in erythrocyte membrane transport in the normotensive offspring of hypertensive parents. Membrane sodium transport was also examined in hypertensive patients whose blood pressure had been controlled by medication. In this group it was found that erythrocyte sodium transport did not differ from that in our control group, which suggests that treatment of hypertension can modify fundamental pathophysiologic changes at the level of the cell membrane.
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PMID:Erythrocyte membrane sodium transport in patients with treated and untreated essential hypertension. 630 25

Ouabain was infused into the third cerebral ventricle of fully conscious, pentobarbital-anaesthetized or urethane-anaesthetized rats. Convulsive seizures occurred in the freely moving rats. The blood pressure of the pentobarbital-anaesthetized rats rose inconsistently. However, in those animals, anaesthetized with urethane, a consistent cardiovascular response was observed with an initial bradycardia, followed by a progressive increase in both the blood pressure and the heart rate. The hypertension was associated with a rise in the CSF potassium level. Tachyphylaxis to these responses was observed.
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PMID:Central hypertensive effect of ouabain in rats. 632 6

Sodium-lithium countertransport (SLC), sodium-potassium cotransport (CoT), and ouabain binding to sodium-potassium adenosine triphosphatase (Na, K-ATPase) sites were measured on fresh erythrocytes from hypertensive and normotensive Utah subjects with and without a first-degree relative with hypertension. SLC was measured as Li+ efflux into NaCl and MgCl2 media from Li+-loaded cells (5-7 mM). CoT was measured by monitoring Na+ and K+ efflux from cells loaded to 20-30 mM Na+ and 20-30 mMK+. Ouabain binding was determined for fresh cells using 3H-ouabain. Subjects were selected from pedigrees that showed a prevalence of hypertension. SLC was significantly elevated in 26.5% of the hypertensive subjects (p less than 0.001) as well as in 12.8% of the normotensives with a hypertensive first-degree relative (p less than 0.05). Although elevated SLC and decreased CoT have previously been associated with hypertension, no hypertensive subject in this study exhibited both abnormalities. All subjects with elevated SLC had normal CoT. A positive correlation between SLC and CoT was observed. Few hypertensive subjects (11.8%) had decreased CoT. In the majority of subjects studied, both SLC and CoT were normal: hypertensives 61.8%, normotensives with a hypertensive first-degree relative 61.7%, and other normotensives 58.7%. The number of ouabain-binding sites was not significantly altered among hypertensives, or their relatives, even though there was a positive correlation between SLC and the number of ouabain-binding sites.
Hypertension
PMID:Three red cell sodium transport systems in hypertensive and normotensive Utah adults. 632 14

We have reported increases in ouabain-sensitive Rb+ uptake by freshly excised conduit arteries from volume-expanded Dahl salt-sensitive (S) rats and also from rats with chronic (4 to 6 weeks), benign (serum creatinine less than 1.4 mg%) one-kidney, one clip ( 1K1C ) hypertension on high NaCl intake. To assess in vivo arteriolar function in this latter model, and a role for putative circulating ouabain-like factors, we perfused the maximally vasodilated (nitroprusside, 0.015 mg/ml limb blood), vascularly isolated, innervated hindlimb vascular beds of chloralose-anesthetized, water- or saline-drinking 1K1C hypertensive rats with their own blood at 1 ml/min, and measured limb responses to i.a. norepinephrine 0.004 to 128 micrograms, before and during local infusion of ouabain (achieving 2.5 X 10(-5) M in limb blood). Complete dose-response curves in eight 1K1C hypertensive rats were steeper and higher than those in five uninephrectomized (1K) normotensive control rats. However, threshold and ED50 were unchanged. Thus, alterations in the curve in the hypertensive rats represented only structural vascular changes. Ouabain evoked a leftward shift of the dose-response curve in an additional 18 1K1C hypertensive rats and 13 1K normotensive controls. In the hypertensive rats as compared to the controls, there were trends for increases, rather than decreases, in the ouabain-induced shift of the curve. Shifts in 14 rats with chronic 2K1C hypertension did not differ from those in the 1K1C hypertensive rats. Together, these studies in chronic, presumably volume-expanded, low-renin hypertension unaccompanied by renal insufficiency provide no evidence for physiologically significant inotropic effects of circulating ouabain-like pump inhibitor.
Hypertension
PMID:Effect of ouabain on arteriolar responses to norepinephrine in chronic, benign, volume-expanded hypertension. 632 25

Red cell sodium and potassium concentrations, and total ouabain-sensitive and ouabain-insensitive first order red constants for sodium efflux, were measured in 15 patients (11 female, 4 male) with essential hypertension (162 +/- 14/99 +/- 7 (s.d. mmHg) and 15 normotensive control subjects (117 +/- 17/64 +/- 10 mmHg) individually matched for age (45.8 +/- 10 versus 45.7 +/- 10 years, respectively, sex, weight (68.6 +/- 16.1 versus 64.7 +/- 11.2 kg) and blood group. To test for possible plasma inhibitors of sodium transport in hypertension, total efflux rate constants were measured in red cells incubated in two plasma samples, from either the same or the complementary (paired) subjects, respectively. Intracellular sodium was significantly increased in patients (11.8 +/- 3.45 versus 8.75 +/- 2.48 mmols/l of red cell water; P = 0.023). Intracellular potassium and total and ouabain-sensitive sodium efflux rate constants, were similar in both groups. Sodium efflux was similar when cells were incubated in the homologous and complementary plasma samples. Ouabain-insensitive rate constants were decreased in the patients (0.16 +/- 0.08 versus 0.20 +/- 0.05 h-1) but the difference was of borderline significance (P = 0.059). These results confirm the presence of abnormal intracellular sodium concentrations and membrane transport in essential hypertension but are not consistent with the suggestion that the abnormalities are due to a circulating sodium transport inhibitor.
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PMID:Evidence against a circulating ouabain-like transport inhibitor as a cause of increased red cell sodium in essential hypertension. 659 99

The effect of local infusion of ouabain into the forearm vascular bed has been examined in 15 normotensive male volunteers in an attempt to define the nature of the functional abnormalities of the resistance vessels in primary hypertension. Ouabain and other drugs were infused into the brachial artery and forearm blood flow was measured by venous occlusion plethysmography. Infusion of ouabain at 2 micrograms/min for 1 h caused a 26% reduction in forearm blood flow with a small rise in systemic arterial pressure; the increase in vascular resistance was unaffected by prior treatment with phentolamine. After infusion of ouabain the dilator response to potassium was reduced by 33% but the responses to verapamil and sodium nitroprusside were unchanged. The results show that acute depression of sodium pump activity by ouabain reproduces the increased resting resistance and impaired response to potassium that are seen in hypertension. It does not reproduce the relative enhancement of responsiveness to verapamil that is also observed in the resistance vessels of patients with hypertension and this abnormality must have some other cause.
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PMID:Effect of local infusion of ouabain on human forearm vascular resistance and on response to potassium, verapamil and sodium nitroprusside. 668 Oct 36

Erythrocyte contents and ouabain-insensitive transport pathways were measured in 120 white and black normotensives and hypertensives. Mean maximal sodium-stimulated lithium-sodium countertransport rate was higher in white hypertensives than in white normotensives, and countertransport was significantly positively correlated with mean arterial pressure in whites. Values similar to those in white normotensives were found in both black normotensives and hypertensives, and countertransport was not significantly correlated with blood pressure in blacks. The rate constant for passive lithium efflux was greater in whites as compared to blacks, and the difference was not related to blood pressure level or sex. Ouabain-insensitive, furosemide-sensitive sodium and potassium effluxes were not found to be altered in hypertension. Furosemide-sensitive sodium efflux rate was lower in blacks but furosemide-sensitive potassium efflux was not similarly depressed. While white subjects demonstrated a close correlation between sodium and potassium effluxes, blacks did not. Further study of these differences in the cellular metabolism of sodium and potassium may provide clues to the pathogenesis of racial dissimilarities in total body sodium handling.
Hypertension
PMID:Racial differences in erythrocyte cation transport. 669 41

86Rubidium influx and Na--K-cotransport have been investigated in erythrocytes of mild essential hypertensives and normotensives devoid of familial hypertension. For measurement of cotransport Na-loaded/K-depleted erythrocytes were used while rubidium influx (with and without ouabain) was determined under physiological conditions. Both transport systems were linear in time, the interassay variances in a range of about 10%. The patients with essential hypertension exhibited a decreased rubidium influx compared to the normotensive controls. Ouabain-sensitive fluxes were not significantly different between the two groups, whereas ouabain-resistent rubidium influx was diminished in the group of the patients. Na--K-cotransport was also found to be decreased in essential hypertension. There was no correlation between cotransport and Rb-influx. The results indicate changes in cation fluxes in erythrocytes of essential hypertensives, the Na--K-cotransport being rather more altered than rubidium influx. It is speculated that hypertensive persons with reduced rubidium flux rates may represent a subpopulation of essential hypertension and that their high blood pressure may be additionally influenced by exogeneous factors e.g. enhanced sodium uptake.
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PMID:[Cation flux in erythrocytes of patients with essential hypertension]. 687 84

1. Ouabain-sensitive 86Rb uptake was used to assess sodium-potassium pump activity in vascular smooth muscle of animals with various types of experimental hypertension. 2. The findings suggest that pump activity is suppressed in the non-genetic low renin, presumably volume-expanded forms of hypertension. 3. By contrast, pump suppression does not appear to be involved in spontaneously hypertensive rats or in salt-induced hypertension in Dahl's salt-sensitive rats. In these genetic models the primary defect may be increased cell membrane permeability.
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PMID:Vascular sodium-potassium pump activity in various models of experimental hypertension. 744 56


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