Beta‐adrenoceptor responsiveness in hypertension: effects of dietary NaCl intake.

Abstract

1. Adrenergic responsiveness may be an important determinant of peripheral resistance in man. We have demonstrated that vascular beta-adrenergic responsiveness is reduced in young borderline hypertensive subjects. A parallel defect in beta-adrenergic mediated adenylyl cyclase activity and beta-adrenoceptor affinity for agonists also has been identified in lymphocytes from borderline hypertensive subjects. In contrast, it is unclear whether cardiac beta-adrenergic responsiveness is altered. 2. The reduction in lymphocyte and vascular beta-adrenergic responsiveness is corrected when hypertensive subjects are fed a low sodium chloride diet. This pattern of regulation differs from that seen in young normotensive subjects fed a low NaCl diet where either reduced or unchanged beta-adrenergic responsiveness has been reported. 3. These studies suggest a generalized defect in beta 2-adrenergic responsiveness in borderline hypertensive subjects and demonstrate important differences between normotensive and hypertensive subjects in the pattern of beta-adrenoceptor regulation mediated by dietary sodium intake. The mechanism by which dietary sodium modulates beta-adrenergic responsiveness is yet to be determined.