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β‐Adrenergic responsiveness is regulated selectively in hypertension
Author(s) -
Feldman Ross D,
Freeman David J,
Bierbrier Gordon S,
Anthony Susan E,
Brown James E
Publication year - 1993
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/clpt.1993.203
Subject(s) - verapamil , blood pressure , medicine , hydrochlorothiazide , endocrinology , adrenergic , placebo , pharmacology , receptor , calcium , alternative medicine , pathology
β‐Adrenergic receptor responsiveness is impaired in hypertension. A low‐sodium diet both corrects this defect and lowers blood pressure. To determine whether upregulation of β‐adrenergic receptor function in hypertension might be related nonspecifically to lowering of blood pressure, vascular β‐adrenergic response was assessed after pharmacologic antihypertensive treatment by use of dorsal hand vein linear differential transformer techniques in patients with hypertension. Subjects were studied after randomized treatments with placebo and verapamil and after randomized treatments with verapamil and hydrochlorothiazide. After 2 weeks of treatment, verapamil lowered blood pressure in the subjects with hypertension but did not significantly upregulate vascular β‐adrenergic response (58% ± 8% to 68% ± 8%; p > 0.2 versus placebo). Further vascular β‐adrenergic responsiveness after treatment with hydrochlorothiazide did not significantly differ from that with verapamil (hydrochlorothiazide, 68% ± 9%; verapamil, 53% ± 7%; n = 8, p > 0.3). Thus, reduction of blood pressure with either verapamil or hydrochlorothiazide did not correct the defect in β‐adrenergic responsiveness in hypertension. Vascular β‐adrenergic response appears to be regulated selectively in hypertension, not simply by lowering of blood pressure. Clinical Pharmacology and Therapeutics (1993) 54 , 654–660; doi: 10.1038/clpt.1993.203