To investigate the cardiovascular effects of bradykinin (BK), the peptide was injected into 6 normotensive volunteers in the supine position. BK was given intravenously as a bolus in a dose of 0.001–7.5 µg BK/kg body weight. Intraarterial blood pressure decreased dose related in a range of 0.25–1.0 µg BK/kg body weight. Pretreatment with 2 × 50 mg indomethacin or 80 mg propranolol as well as changes in oral salt intake (from 10 to 300 mmol NaVday) had no effect on the blood pressure-lowering effect of BK. Captopril (25 mg) potentiated the effect of BK 20- to 50-fold. In primary hyperaldosteronism, renal kallikrein activity and absolute vascular reaction to BK was increased. The results showed clearly that in man, similarly as in rats, BK lowers blood pressure by direct vasodilation and acts independently of prostaglandins, β-receptors or salt intake.