Furosemide-sensitive sodium and potassium cotransport and intracellular sodium content ([Na],) were measured in erythrocytes (red blood cells, RBCs) from a population of 90 adult black men with and without essential hypertension (EH). The mean values for sodium cotransport activity, expressed as furosemide-sensitive Na efflux (mmol/liter RBC/hr), were not significantly different among the EH patients and two control groups, normotensive subjects with a positive history (N + ) and those with a

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... and those with a negative family history (N-) for hypertensive disease (EH: 154 ± 123, n = 53; N+:167 ± 93, n = 12; and N~: 207 ± 142, n = 20; all values are means ± SD). The mean [Na], 9.66 ± 3.02 mmol/liter RBC (n = 56) for the EH group was greater than the mean value for the N~ control group (7.96 ± 1.97, n = 20; p < 0.05). The N+ group also displayed a higher mean [Na], (10.38 ± 3.18, n = 12; N + vsN~ p< 0.01). Although there was substantial overlapping of [Na], values between the groups and no clear dividing line, the distribution curve of the [Na], values in EH was skewed toward higher concentrations than in N~. Nevertheless, we must conclude that erythrocyte cotransport and [Na], are not clinically useful in the identification of EH in black men. (Hypertension 6: 724-730, 1984) KEY WORDS • essential hypertension • sodium • erythrocyte E SSENTIAL hypertension (EH) is a major public health problem in industrialized countries. It is generally accepted that heredity plays an important role in the etiology of EH although the extent of involvement is still unresolved. 1 Studies 2 in strains of rats that become hypertensive on high salt diets (Dahl salt-sensitive rats) have demonstrated a genetically transmitted defect of renal sodium (Na) excretion, the hypertensive effects of which are humorally mediated. The cellular factors responsible for the Na excretion deficiency have not been identified, but the involvement of renal cellular cation transport From the Division of Pediatric Cardiology