Low sodium diet corrects the defect in lymphocyte beta-adrenergic responsiveness in hypertensive subjects.
AUTOR(ES)
Feldman, R D
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=424047Documentos Relacionados
- Defective venous beta-adrenergic response in borderline hypertensive subjects is corrected by a low sodium diet.
- Beta-adrenergic function in airways of healthy and asthmatic subjects.
- Regulation of cardiac sodium-calcium exchanger by beta-adrenergic agonists.
- Interleukin 1 prevents loss of corticotropic responsiveness to beta-adrenergic stimulation in vitro.
- Interleukin 1 and tumor necrosis factor inhibit cardiac myocyte beta-adrenergic responsiveness.