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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The number of sodium pump units of erythrocytes measured with ouabain binding assay was significantly lower in 17 patients with essential hypertension (0.538 +/- 0.020 pmol/10(9) cells) than in 13 normotensive controls (0.673 +/- 0.031 pmol/10(9) cells) (p less than 0.01) and it was inversely correlated with erythrocyte sodium concentration (r = -0.86, p less than 0.01).
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PMID:Reduced number of erythrocyte sodium pump units in essential hypertension. 609 Dec 95

Sodium efflux rates were measured in leucocytes from eighteen normotensive subjects who had one or more first-degree relatives with essential hypertension and from twenty-four matched controls with no such family history. The total efflux rate constant was significantly lower in those with a family history of hypertension, owing to reduced ouabain-sensitive sodium pump activity. The presence of a membrane electrolyte handling abnormality characteristic of essential hypertension in normotensive individuals genetically predisposed to hypertension points to an underlying genetic factor. At the same time, the fact that blood-pressure was normal in these subjects indicates that the abnormality does not participate directly in blood-pressure elevation. Rather, the abnormality, like other red-cell changes in electrolyte handling, seems to be a marker for a genetically determined alteration in membrane structure, and thus only indirectly related to hypertension.
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PMID:Leucocyte membrane sodium transport in normotensive populations: dissociation of abnormalities of sodium efflux from raised blood-pressure. 612 51

The presence in plasma extracts of a sodium pump inhibitor with digitalis-like properties was investigated by two complementary tests: decrease in the affinity of ouabain binding to human red blood cells and inhibition of Na+,K+-ATPase. The results of the two methods were correlated (r = 0.76, n = 44, p less than 0.01), suggesting that the same factor may be responsible for both effects. All subjects with elevated values were hypertensive or normotensive and had a family history of hypertension. Forty percent of the subjects in these two groups had high inhibition values. The elevation was significant (p less than 0.01) when compared with values in normotensive subjects with no hypertensive heredity. Increased inhibition was observed in patients taking beta-blocking agents; conversely, diuretics normalized the values. No correlation was found between pump inhibition and age, sex, blood pressure, levels of plasma K+ or Na+, or plasma renin activity. These data show the existence of a sodium pump inhibitor in the plasma of some subjects and point to a possible association with hypertension. They also underline the importance of genetic background and the heterogeneity of essential hypertension.
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PMID:Plasma sodium pump inhibitor in essential hypertension and normotensive subjects with hypertensive heredity. 620 59

A digitalis-like compound was detected in human plasma by tritiated ouabain competition binding to the sodium pump. The study comprised analyses of plasma extracts from 17 normal controls, 17 normotensive subjects with one or both parents hypertensive, and 16 patients with untreated essential hypertension. In two thirds of the untreated hypertensive and several of the normotensive subjects with a family history of hypertension the potency of the digitalis-like compound, as measured by its interference with ouabain binding, was significantly greater than in the controls. In the untreated hypertensive patients the potency of the compound was significantly correlated with the urinary sodium output. Measurement of this salt-related, digitalis-like compound may be useful in clinical studies of hypertension.
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PMID:Measurement of digitalis-like compound in plasma: application in studies of essential hypertension. 630 18

Subnormal activity of the Na+-K+-ATPase appears to be a common feature of essential hypertension, and may in fact play a pathogenic role in this disorder. If so, methods which relieve inhibition or enhance the activity of the sodium pump should have therapeutic or preventive value. Diuretics enhance the activity of the sodium pump in hypertensives, apparently by suppressing secretion of an inhibitory natriuretic factor, and it is likely that low-sodium diets have a similar effect. Activity of the Na+-K+-ATPase is also stimulated by thyroid hormone and insulin, and there are indications that thyroid therapy, as well as various measures which increase tissue insulin sensitivity, may have therapeutic value in essential hypertension. Nutritional measures which may enhance sodium pump activity include potassium supplementation, insurance of adequate magnesium intake, and consumption of rich sources of gamma-linolenic acid.
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PMID:Hormonal and nutritional enhancement of Na+-K+-ATPase activity may aid the prevention and treatment of essential hypertension. 632 33

In this review, postulated passive and active fluxes of sodium, potassium, and calcium across the sarcolemma of the normal vascular smooth muscle cell are first summarized. Some practical problems encountered in their measurement are also mentioned. The review then considers how these fluxes appear to be altered in various forms of hypertension in animals and humans. Emphasis is given to abnormal fluxes of sodium and potassium due to altered sodium pump activity and permeability. Increasing evidence indicates that sodium retention due to increased sodium intake or decreased sodium excretion causes hypertension by releasing a humoral pressor substance from brain. This substance, which may be the putative natriuretic hormone, inhibits Na+, K+-ATPase and sodium pump activities in blood vessels and heart, thereby increasing contractile activity. In the genetic models of hypertension, the primary defect appears to be increased permeability of the vascular smooth muscle cell wall to sodium; pump activity increases to compensate for the increased inward leak of sodium. This may also be the case in patients with heritable essential hypertension. The possible consequences of super-imposing the sodium pump inhibitor on the primary defect are also considered. This may occur when animals with genetic hypertension or patients with heritable essential hypertension retain sodium subsequent to increased sodium intake and/or decreased ability to excrete sodium. Such superimposition should raise intracellular sodium concentration to high levels since now the pump would not fully compensate for the increased inward leak of sodium.
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PMID:Abnormalities of membrane transport in hypertension. 636 Aug 83

It has been postulated that depressed membrane sodium transport is a necessary step in blood pressure elevation in essential hypertension. Accordingly, leucocyte sodium efflux-rate constants were estimated in 14 normotensive subjects who had one or more first-degree relatives with essential hypertension, and also in 14 matched control subjects with no such family history, before and after taking bendrofluazide for 7 days. Efflux rates in the controls did not change after the diuretic. However, in the relatives, mean total sodium efflux-rate constant was at first significantly depressed but later rose to normal with the diuretic. This was due almost entirely to an increase in glycoside-sensitive sodium pump activity. Blood pressure remained unchanged in both groups. Thus, assuming that perturbations in leucocytes reflect similar abnormalities in other cell lines, major changes in sodium transport in the normotensive individual without accompanying changes in blood pressure suggest that, while these changes may be a marker for later hypertension, they do not participate directly in blood pressure control.
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PMID:Changes in leucocyte sodium transport in normotensive relatives of hypertensive subjects. Dissociation from blood pressure. 637 43

Leucocyte sodium efflux rate constants and intracellular electrolyte contents were estimated in 13 patients with untreated essential hypertension. There was no correlation between intracellular sodium or potassium content or efflux rate constant and blood pressure. The patients were then treated with oral nifedipine and blood pressure controlled. Sodium efflux rate constants and electrolyte contents were estimated one and three months after the start of treatment. There was a significant fall in blood pressure, but mean sodium efflux rate constant and intracellular sodium content were unchanged. There was no correlation between the fall in blood pressure, initial sodium efflux, or intracellular sodium content. These data do not support the hypothesis that the sodium pump and intracellular sodium content have a direct role in generating raised blood pressure, or that treatment of hypertension with calcium antagonists corrects a fundamental alteration of calcium-sodium exchange across the cell membrane.
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PMID:Calcium antagonists in hypertension: relation to abnormal sodium transport. 641 34

Various functions of erythrocytic cation transport were studied in normotensive and hypertensive pregnancy (women with pre-eclampsia and essential hypertension). The results showed that in pregnancy there is an increase in the number of erythrocytic glycoside binding sites accompanied by a proportional increase in the active inward transport of rubidium (used as a substitute for potassium). There was no evidence of an effect of pregnancy on intraerythrocytic sodium concentrations. These changes were apparently entirely attributable to pregnancy and not affected by pre-eclampsia or essential hypertension. It is suggested that these alterations indicate an adaptive increase in sodium pump numbers and activity secondary to a tendency for the intraerythrocytic sodium concentration to rise during pregnancy and compensating for that tendency.
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PMID:Erythrocytic cation transport receptor numbers and activity in pregnancies complicated by essential hypertension and pre-eclampsia. 642 46

Leucocytes were isolated from venous blood of 11 normotensive volunteers with no family history of hypertension and the sodium efflux rate constants determined both alone and in the presence of increasing physiological concentrations of noradrenaline. There was a significant dose dependent reduction of total sodium efflux rate constant due to a reduction in ouabain sensitive sodium pump activity, glycoside insensitive efflux rate constants being unaffected. The magnitude of this effect was similar to the reduction in leucocyte sodium efflux rate constants observed in hypertensive patients (and their normotensive relatives). The noradrenaline induced depression of sodium pump activity was prevented by propranolol in a further seven experiments, suggesting that the effect was mediated by beta adrenoceptors. Catecholamines possibly functioning as circulating inhibitors of sodium transport may contribute to some of the disturbances in membrane electrolyte handling both in essential hypertension in man and in some experimental models of hypertension.
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PMID:Noradrenaline: a circulating inhibitor of sodium transport. 643 58


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