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

An increase in intra-erythrocytic sodium (IENa) content has been proposed as a genetic marker of essential hypertension. Intra-erythrocytic sodium was studied using hypotonic lysis and flame photometry after four washings with isotonic MgCl2 in 240 normotensive subjects (aged 10-45 years) on a free diet with (F+, 121 patients) or without (F-, 119 patients) hypertensive parents, recruited from a random sample of the general population. Systolic blood pressure was significantly higher in males F+ than in males F- (130 +/- 2 versus 125 +/- 2 mmHg, mean +/- s.e.m., P < 0.05), while IENa did not differ. In contrast, intra-erythrocytic potassium content (IEK) was significantly lower and red cell sodium potassium (Na:K) ratio significantly higher in F+ than F-. This might reflect decreased NaK pump activity, or increased membrane permeability to cations which causes increased K leakage. No differences in blood pressure, IENa or IEK showed in female F+ versus F-. It is concluded that IENa is not a genetic marker of hypertension, and that it is probably influenced by exogenous factors. Being associated with differences in blood pressure, the abnormalities of IEK and Na:K ratio might be pathogenetically linked to an early increase in blood pressure.
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PMID:Intra-erythrocytic sodium content in normotensive offspring of normotensive and hypertensive subjects: an epidemiological study. 285 84

The activity and some allosteric properties of Na+-K+-ATPase in erythrocytes and their membrane preparations (ghosts) from 57 patients with essential hypertension and 36 normotensive controls were studied. To reveal enzyme activity in whole erythrocytes the cells were pretreated with detergent Tween-20. It was found that in the patient erythrocytes the Na+-K+-ATPase activity was 33% less as compared to the control group. Moreover, in the patient erythrocytes the sensitivity of the enzyme to high concentrations of MgCl2 was decreased. In contrast, no analogous changes of the enzyme were revealed in the patient ghosts. It is suggested that the erythrocytes of patients with essential hypertension contain an inhibitor of Na+-K+-ATPase.
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PMID:Some properties of erythrocyte Na+-K+-ATPase in essential hypertension. 304 Mar 5

To investigate the pathophysiology of essential hypertension, detailed biochemical and clinical variables were collected and analyzed for 2091 Utah subjects aged 3 to 83 years. Three different measurements of erythrocyte cation transport were obtained: Na+-Li+ countertransport, Li+-K+ cotransport, and furosemide-insensitive Li+ efflux into MgCl2. Total plasma cholesterol, triglycerides, and high density lipoprotein cholesterol levels were obtained from fasting subjects. Levels of high density lipoprotein subfractions 2 and 3 were also obtained from 350 subjects. Standardized data collection also included blood pressure, height, weight, and presence or absence of a diagnosis or treatment of essential hypertension. In univariate analyses of all 1420 adults, each of the three transport systems showed the same significant correlations with triglyceride levels (r = 0.33-0.35, p less than 0.0001), high density lipoprotein concentration (r = -0.19 to -0.21, p less than 0.001), and weight (r = 0.22-0.28, p less than 0.0001). In multivariate regression analyses, values for each transport system were significantly higher in hypertensive subjects; values for triglycerides, high density lipoprotein, and usually, the high density lipoprotein subfractions continued to have strong significant independent associations with all three transport systems; and weight remained significantly related only to Na+-Li+ countertransport. In separate logistic regressions, plasma triglyceride levels (positively, p less than 0.001) and high density lipoprotein subfraction 3 levels (inversely, p less than 0.03) were associated with hypertension itself. In multivariate analyses among 671 children, high density lipoprotein and high density lipoprotein subfraction 3 levels showed significant (p less than 0.05) inverse correlations with Na+-Li+ countertransport and furosemide-insensitive Li+ efflux.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Associations of three erythrocyte cation transport systems with plasma lipids in Utah subjects. 394 85

Ouabain-resistant Na and Li effluxes in erythrocytes from 18 normal subjects and 19 hypertensive subjects were studied in fresh cells that contained about 9 mmol Li and 2.5 or 6.5 mmol Na per liter of erythrocytes after intact cells had been incubated for 5 hours in 110 mM Li, 40 mM Na medium, with or without ouabain 10(-4) M. Outward Na cotransport was estimated at both internal Na concentrations as the furosemide-sensitive unidirectional 22Na efflux from erythrocytes into a Na free-medium containing 75 mM MgCl2. The changes in furosemide-sensitive outward Na transport between the two levels of internal Na were considered as a measure of the response of Na cotransport to the changes in internal Na within its physiological range. At both levels of internal Na, outward Na cotransport was reduced in the majority but not in all of the patients with essential hypertension (p less than 0.05 at 2.5 mmol; p less than 0.001 at 6.5 mmol). The ratio of the changes in Na cotransport to those in internal Na was lower in the hypertensive patients than in the control subjects (17.2 mumol/liter red blood cells/hr/1 mmol in internal Na increase vs 42.2, p less than 0.001). The Li-Na countertransport was increased in a few patients with essential hypertension, with no relationship to cotransport. We conclude that, in essential hypertension, the outward Na + K cotransport is impaired in fresh erythrocytes not treated with PCMBS (2,5 p-chloromercuribenzene sulfonate) or nystatin, even when internal Na is around its physiological range.
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PMID:Low sodium cotransport in red cells with physiological internal sodium concentration in essential hypertension. 609 41

Abnormal cellular ion transport resulting in altered membrane control over intracellular calcium may be aetiologically related to essential hypertension. Cell membrane calcium binding, which is influenced by magnesium, is an important membrane system involved in cellular calcium regulation. In this study the relationships between erythrocyte calcium binding and extra- and intracellular calcium and magnesium concentrations were determined in essential hypertensive patients (52 black, 24 white) and normotensive controls (52 black, 26 white). Calcium depletion of the erythrocytes by MgCl2 and EDTA resulted in the removal of more calcium ions from the outer erythrocyte membrane in the hypertensive group compared with the normotensive group. This may be considered as evidence of increased calcium binding to the outer cell membrane in essential hypertension. Calcium binding was greater in the hypertensive males compared with the females. In black hypertensives, serum and erythrocyte magnesium concentrations were significantly increased. In white hypertensives, serum calcium was significantly decreased and erythrocyte calcium significantly raised. Serum and erythrocyte magnesium correlated inversely with the amount of calcium released from the membranes in the black hypertensive group. The results of this study suggest that changes in magnesium levels may contribute to altered cell membrane calcium binding in essential hypertension.
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PMID:Altered calcium binding to erythrocyte membranes in essential hypertension: relation to magnesium. 845 May 22