The bolus ip. administration of a SRIF antagonist (SRIF-A) (60 nM/rat) significantly increased renin activity (PRA) and plasma aldosterone concentration (PAC) in rats, without affecting natremia, kalaemia and the blood levels of ACTH or corticosterone. SRIF-A also raised PAC in rats whose renin-angiotensin system had been pharmacologically interrupted by combined captopril/angiotensin-II infusion and in which PRA was very low. The ip. injection of an equimolar dose of SRIF completely reversed these effects of SRIF-A, but the administration of SRIF alone did not affect either PRA or PAC. Taken together, these data would suggest that, in the rat, endogenous SRIF exerts, under basal conditions, a two-fold maximum tonic inhibitory effect on both renin release by kidneys and aldosterone secretion by zona glomerulosa cells.