Does chronic alpha- and beta-adrenergic receptor blockade reduce plasma renin activity in normal and hypertensive adults?
Beta-adrenergic blockade significantly suppresses plasma renin activity without necessarily lowering blood pressure, indicating that factors other than renin are involved in the pathogenesis of renal hypertension.
The response of plasma renin activity (PRA) to the stimuli of upright posture and sodium deprivation was determined in three normal adults and in ten hypertensive patients before and after chronic alpha-adrenergic receptor blockade with phenoxybenzamine and chronic beta-blockade with propranolol. Alpha-receptor blockade produced little effect on supine or upright PRA values; beta-receptor blockade, however, consistently and significantly suppressed PRA in both the supine and standing positions. Dose-response studies suggest that the maximal suppression of PRA attainable after oral propranolol administration occurs at peak plasma levels of about 30–50 ng/ml. Beta-adrenergic receptors appear to constitute that part of the sympathetic nervous system which mediates a significant portion of the renin release mechanism. Pharmacologic interference with renin secretion by beta-adrenergic receptor blockade is easily achieved in both normal and hypertensive subjects. The suppression of supine and upright PRA with beta-adrenergic blockade was not accompanied by decrease in blood pressure suggesting that, in addition to renin, other factors are involved in the pathogenesis of renal hypertension.
Michelakis et al. (1972) studied this question.