Low sodium diet corrects the defect in lymphocyte β-adrenergic responsiveness in hypertensive subjects

Abstract

To determine the role of dietary sodium intake in the reduction in β-adrenergic sensitivity in hypertension, lymphocyte β-receptors from 8 borderline hypertensive and 16 normotensive subjects were studied after 5 d on a high sodium diet (400 meq/d) and also following a low sodium diet (10 meq/d). During the high sodium diet, lymphocyte β-receptor-stimulated adenylate cyclase activity, expressed as the relative increase over basal levels stimulated by the β-agonist isoproterenol, was significantly (P < 0.025) decreased in hypertensive (24 ± 5%, mean ± SE) compared with normotensive (42 ± 4%) subjects. Neither β-receptor density nor the proportion of nonsequestered β-receptors differed between groups. A low sodium diet significantly increased β-receptor-stimulated adenylate cyclase activity in hypertensives (low sodium, 51 ± 7%; high sodium, 24 ± 5%, P < 0.025) to a level not different than that of normotensives (46 ± 5%). Thus, reduced lymphocyte β-receptor responsiveness in hypertensive subjects is not due to β-receptor sequestration and is corrected on a low sodium diet. Dietary sodium may be an important factor in the β-receptor defect in early hypertension.