Beta-adrenoceptor responsiveness in hypertension: effects of dietary NaCl intake.
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.
Feldman
R D
RD
Department of Medicine, University of Western Ontario, London, Canada.
D000818:Animals; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000378:metabolism*; D012982:Sodium, Dietary / Q000494:pharmacology*
D011943:Receptors, Adrenergic, beta; D012982:Sodium, Dietary