Captopril-induced gastric motor response, reflected as change in intragastric pressure (IGP) in rats under urethane anaesthesia, was investigated. Single injection (i.v.) of captopril decreased the gastric motor tone in 2 distinct phases: a transient (6-10 min) short-latency relaxation (SLR) was followed by a long-lasting (1 hr) delayed relaxation (DGR). The SLR coincided with the time course of simultaneously evoked changes in the cardiorespiratory parameters by captopril. Neither phase of the gastric relaxation exhibited dose-dependency. The kallikrein inhibitor, aprotinin markedly attenuated both phases of the relaxation, the angiotensin II antagonist saralasin was without significant effect. The DGR was sensitive to subdiaphragmatic vagotomy, bilateral adrenalectomy, propranolol (3 mg/kg) and indomethacin (10 mg/kg), but resistant to guanethidine (5 mg/kg). The SLR was only partially blocked by vagotomy, guanethidine and indomethacin. It was almost abolished by adrenalectomy, though insensitive to propranolol. It is argued that the captopril-induced gastric relaxation, especially the DGR, is predominantly due to the enhanced endogenous kinin activity which reflexly releases adrenal medullary catecholamines by exciting chemosensitive vagal afferents of abdominal origin. This kinin-induced activation of vagal afferents seems to be mediated by prostaglandins.