This study characterized the alpha-1 adrenoceptor subtypes involved in adrenergically induced antinatriuresis and antidiuresis in pentobarbital-anesthetized deoxycorticosterone acetate (DOCA)-salt and two kidney, one clip (2K1C) Goldblatt hypertensive rats. In the DOCA-salt rats, phenylephrine infusion (100 microgram kg(-1) hr(-1) close renal arterially) caused increases in blood pressure of 5 to 10%, decreases in renal blood flow of 5 to 12%, whereas there were large reversible decreases in urine flow and absolute and fractional sodium excretions of 55 to 70%. The presence of chloroethylclonidine (10 microgram kg(-1) hr(-1) to block alpha-1B adrenoceptors) had no effect on the magnitude of the phenylephrine-induced excretory responses, but after 5-methylurapidil (10 microgram kg(-1) hr(-1) to block alpha-1A adrenoceptors) they were abolished. Infusion of phenylephrine in the 2K1C hypertensive rats caused small hemodynamic and renal blood flow responses with marked 55 to 70% reductions in urine flow and absolute and sodium excretion. The phenylephrine-induced antinatriuresis and antidiuresis, which was probably due to activation of alpha-1 adrenoceptors present on the renal tubular epithelial cells, and the fact that these tubular responses were blocked by 5-methylurapidil but not by chloroethylclonidine in both DOCA-salt and 2K1C Goldblatt hypertensive models, means that the alpha-1A adrenoceptors was the major functional subtype present.