The effect of captopril (SQ 14,225) on the renal hemodynamics, cortical plasma flow (CPF) and noncortical plasma flow (NCPF), was studied in sodium-replete anesthetized dogs during aprotinin infusion. Mean blood pressure (MBP) increased by aprotinin (p less than 0.05) and decreased by captopril (p less than 0.02). Renal vascular resistance (RVR) tended to increase by aprotinin and decreased from 1.29 to 0.86 mm Hg/ml/h (74.7%) by captopril (p less than 0.05). Renal vein renin activity (RRA) inclined to decrease by aprotinin and increased from 17.8 to 47.2 ng/ml/h (278.2%) by captopril (p less than 0.05). Although the administration of captopril alone did not alter the renal hemodynamics despite the reduction of MBP, captopril made a recovery of renal plasma flow (RPF), CPF and NCPF which had decreased by aprotinin. Especially, CPF showed a significant recovery from 45.4 to 55.6 ml/min (123.6%) by captopril (p less than 0.02). These results indicate that the inhibition of endogenous angiotensin made a preferential increase in CPF and suggest that the renin-angiotensin system plays a major role in the effect of captopril of the renal hemodynamic changes.