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

作者: R D Feldman , W J Lawton , W L McArdle

DOI: 10.1172/JCI112797

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

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