Bradykinin is one of the most potent vasodilators and in the kidney it develops a marked diuretic and natriuretic action. The natriuretic effect of the peptide is mediated by prostaglandins. The mechanism of bradykinin induced vasodilation, however, is not yet known. Therefore, in this study the blood pressure lowering effect of bradykinin was investigated in five normotensive volunteers. Bradykinin was injected intravenously in doses between 0.001 and 7.5 micrograms/kg of body weight. Intraarterially measured blood pressure decreased in a dose related manner from 0.25 to 1.0 micrograms/kg. Changes in oral salt intake (10 to 300 nmol Na+/d) had no effect on the action of bradykinin as well as pretreatment with either indomethacin (2 X 50 mg) or propranolol (80 mg). Captopril (25 mg) potentiated the blood pressure lowering effect of bradykinin about 20-fold. In four patients with renal hypertension bradykinin provoked a more marked reduction in arterial blood pressure, while potentiation by captopril was not different in the hypertensives if compared to the normotensives. The results of our studies show that bradykinin lowers blood pressure by a direct mechanism, which acts independently of salt intake, beta-receptors and prostaglandins. Inhibition of inactivation of bradykinin by captopril enhances its activity markedly. In renal hypertension the arterial vessels are more sensitive to bradykinin than in normotension, probably indicating a lack of endogenous kinins in these patients.