The role of adrenergic receptors in mediating renin secretion was studied in normal subjects with the use of upright posture and administration of diazoxide, ethacrynic acid and theophylline to provoke renin release. Each of these stimuli produced the expected rise in plasma renin activity (PRA), despite marked differences in their effect on urinary sodium excretion. In each case the increase in PRA was markedly suppressed on retesting with an infusion of either phentolamine, an alpha-adrenergic blocking agent, or propranolol, a beta-adrenergic blocking agent, whereas adrenergic blockade had little or no affect on sodium excretion. Since the stimuli chosen for provoking renin release have diverse mechanisms of action, it is noteworthy that PRA was suppressed by adrenergic blockade, regardless of the stimulus used. These findings suggest that many, if not all, of the stimuli for renin release are mediated by a common pathway which may involve alpha-and beta-adrenergic receptors. Moreover, renin release may occur independently of changes in sodium excretion. (J Clin Endocr 29: 1168

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