Low sodium diet corrects the defect in lymphocyte beta-adrenergic responsiveness in hypertensive subjects.
To determine the role of dietary sodium intake in the reduction in beta-adrenergic sensitivity in hypertension, lymphocyte beta-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 beta-receptor-stimulated adenylate cyclase activity, expressed as the relative increase over basal levels stimulated by the beta-agonist isoproterenol, was significantly (P less than 0.025) decreased in hypertensive (24 +/- 5%, mean +/- SE) compared with normotensive (42 +/- 4%) subjects. Neither beta-receptor density nor the proportion of nonsequestered beta-receptors differed between groups. A low sodium diet significantly increased beta-receptor-stimulated adenylate cyclase activity in hypertensives (low sodium, 51 +/- 7%; high sodium, 24 +/- 5%, P less than 0.025) to a level not different than that of normotensives (46 +/- 5%). Thus, reduced lymphocyte beta-receptor responsiveness in hypertensive subjects is not due to beta-receptor sequestration and is corrected on a low sodium diet. Dietary sodium may be an important factor in the beta-receptor defect in early hypertension.
D000262:Adenylyl Cyclases / Q000378:metabolism; D000328:Adult; D004039:Diet, Sodium-Restricted; D004789:Enzyme Activation / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000178:diet therapy* / Q000503:physiopathology; D008214:Lymphocytes / Q000502:physiology; D011412:Propanolamines / Q000378:metabolism; D011943:Receptors, Adrenergic, beta / Q000502:physiology; D013997:Time Factors
D011412:Propanolamines; D011943:Receptors, Adrenergic, beta; D000262:Adenylyl Cyclases; C033394:CGP 12177