Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rate of lithium, sodium, and potassium transport in red blood cells is thought to be associated with essential hypertension. In order to investigate the contribution of genetic and environmental factors to cation transport, their correlation was analyzed in 60 parent-offspring pairs and 17 husband-wife pairs in Toyama City, Japan. Lithium-sodium countertransport and sodium-potassium cotransport rates were significantly correlated in parent-offspring pairs (r = 0.52, p less than 0.01 and r = 0.46, p less than 0.01, respectively) but not in husband-wife pairs. Sodium pump rates were significantly correlated in both pairs (r = 0.48, p less than 0.01 in parent-offspring pairs, r = 0.46, p less than 0.05 in husband-wife pairs). Therefore, lithium-sodium countertransport and sodium-potassium cotransport were found to have a substantial genetic component and the sodium pump to have a substantial environmental component. Sodium pump rates were significantly correlated with sodium/creatinine (r = 0.21, p less than 0.05) and sodium/potassium (r = 0.32, p less than 0.01) in casual urine.
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PMID:Familial aggregation of red blood cell cation transport systems in Japanese families. 241 Nov 26

In nine young normotensive subjects with no family history of hypertension and nine age-matched normotensive subjects with one parent with essential hypertension, effective renal plasma flow (p-aminohippuric acid clearance), glomerular filtration rate (inulin clearance), and excretion of sodium and exogenously administered lithium were measured for 90 minutes before and after administration of a single 20-mg oral dose of the calcium entry blocker nifedipine. Segmental tubular handling of fluid and sodium was estimated using lithium clearance as a marker of proximal tubular reabsorption. Nifedipine did not cause any change in subjects with no family history of hypertension, but in those with one hypertensive parent there was a marked increase in effective renal plasma flow (from 644 +/- 39 to 847 +/- 42 [SEM] ml/min x 1.73 m2; p less than 0.001) and a decrease in filtration fraction (from 17.6 +/- 1.0 to 12.6 +/- 0.4%; p less than 0.001), while the glomerular filtration rate was unchanged, thus suggesting a prevailing efferent vasodilation. Sodium excretion rate (p less than 0.02) and fractional sodium excretion (p less than 0.025) increased slightly but significantly in subjects with one hypertensive parent, but not in normotensive subjects with no family history of hypertension. Lithium clearance also rose (from 29.0 +/- 2.0 to 32.8 +/- 1.9 ml/min, p less than 0.001), and the derived value of fractional proximal reabsorption diminished (from 75.8 +/- 1.0 to 71.3 +/- 1.2%, p less than 0.001). Estimated distal delivery of sodium and absolute distal sodium reabsorption both increased significantly (p less than 0.005), while fractional distal sodium reabsorption was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormal renal responses to calcium entry blockade in normotensive offspring of hypertensive parents. 284 83

Sodium-dependent lithium efflux was measured in erythrocytes from 399 factory workers and 125 patients attending a hypertension clinic. Thirty-two factory workers had unsuspected essential hypertension (diastolic blood pressure phase V greater than 90 mmHg). These subjects had the same average erythrocyte lithium efflux as those with normal blood pressure, whereas lithium efflux was increased on average in the clinic hypertensives. Lithium efflux was greater in those subjects from both groups who had a family history of high blood pressure. Our clinic hypertensives did not have raised lithium efflux when they were matched for family history; the increased lithium efflux in the group as a whole (and in analysis of published reports) was explained by an excess of subjects with a family history of hypertension. Furthermore, when a family history of hypertension was present, lithium efflux was increased on average only in those whose relatives also had a cardiovascular event associated with their high blood pressure. These results, in conjunction with detailed analysis of the distributions of lithium efflux within the groups, suggest that, though not linked to blood pressure itself, an increase in lithium efflux is an inherited marker for those at risk from the cardiovascular complications associated with high blood pressure.
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PMID:Relations between erythrocyte lithium efflux, blood pressure and family histories of hypertension and cardiovascular disease: studies in a factory workforce and hypertension clinic. 379 34

1. Erythrocyte lithium--sodium countertransport was measured in 46 normotensive healthy controls without family history of hypertension, 15 subjects with essential hypertension, but without evidence of family history of high blood pressure, and 43 subjects with essential hypertension and at least one hypertensive first-degree relative. 2. Mean values (mmol h-1 l-1 of erythrocytes) were 0.248 +/- 0.092 in controls, 0.258 +/- 0.087 in hypertensive subjects without family history (not significant vs controls), 0.360 +/- 0.115 in hypertensive subjects with family history of hypertension (P less than 0.001 vs controls), 0.334 +/- 0.117 in all hypertensive subjects, both with and without family history (P less than 0.001 vs controls). 3. Our data confirm the finding of an increased erythrocyte lithium--sodium countertransport, but with a significant overlap between essential hypertension and control values. Lithium--sodium countertransport is higher only in hypertensive subjects with at least one hypertensive first-degree relative. 4. We suggest that the increase of lithium--sodium countertransport in erythrocytes is not a consistent marker of essential hypertension. It seems to be associated with the family prevalence and/or the hereditability of hypertension, rather than with high blood pressure per se.
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PMID:Increased erythrocyte lithium--sodium countertransport in essential hypertension: its relationship to family history of hypertension. 731 13

We previously showed that children and adolescent offspring of patients with essential hypertension have an increased proximal renal sodium reabsorption as measured by lithium fractional excretion. Insulin has been shown to have antinatriuretic properties and to be increased (hyperinsulinemia) in essential hypertension. The aim of this study was to evaluate the role of insulin on the increased proximal renal sodium reabsorption previously reported. Lithium and sodium fractional excretions were measured 3 hours before and 3 hours after an intravenous glucose tolerance test in 20 normotensive adolescents with a family history of essential hypertension (F+, 14.8 +/- 0.5 years) and 10 normotensive control subjects without a family history of hypertension (F-, 15.2 +/- 0.9 years). Results are mean +/- SEM. Lithium fractional excretion before glucose loading was 16.1 +/- 1.8% in F+ versus 23.5 +/- 2.0% in F- (P < .02) and after glucose loading was 14.7 +/- 1.3% in F+ versus 20.9 +/- 1.7% in F- (P = NS). Lithium fractional excretion did not change after intravenous glucose loading in either group. The insulin area under the curve was 2815 +/- 499 in F+ versus 2290 +/- 418 microU/mL per hour in F- (P = NS). There was no correlation between lithium fractional excretion and insulin area under the curve. Fractional excretion of sodium before glucose loading was 0.99 +/- 0.1% in F+ versus 0.99 +/- 0.1% in F- (P = NS) and after glucose loading was 0.77 +/- 0.1 in F+ versus 0.85 + 0.1% in F- (P < .01 versus values before loading in both groups).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin effect on renal sodium reabsorption in adolescent offspring of essential hypertensive parents. 749 74