1. Administration of captopril (1.5 mg/kg i.v.) to anaesthetized dogs was associated with an increase in renal blood flow of 56 ml min-1 (s.e.m. = 13, n = 9) despite a significant fall of 17 mmHg (s.e.m. = 5, n = 9) in mean arterial pressure. 2. Treatment of dogs with the angiotensin receptor antagonist, Sar1 Ile8-angiotensin II (2.5 micrograms/kg per min i.v.), or the cyclo-oxygenase inhibitor indomethacin (10 mg/kg i.v.) did not prevent the renal vasodilation and hypotension following angiotensin-converting enzyme inhibition. This suggests that these effects are neither solely due to inhibition of the renin-angiotensin system nor mediated by prostaglandins. 3. Increased urinary kinin excretion, possibly reflecting increased renal concentrations of kinins, accompanied the renal vasodilation after both captopril and renal artery occlusion. 4. The kallikrein-kinin system may play a role in the regulation of the renal vasculature in anaesthetized dogs.