The effects of captopril on the forearm hemodynamics in patients with severe congestive heart failure were studied, using strain-gauge plethysmography. To determine whether prostaglandins are involved in the captopril actions, indomethacin, an inhibitor of prostaglandin synthesis, was administered. In 8 patients, captopril (25 mg) decreased mean blood pressure (P less than 0.01) and venous pressure (P less than 0.05); forearm blood flow (P less than 0.05) and maximum venous volume (P less than 0.05) were increased; forearm vascular resistance (P less than 0.05) and forearm venous tone (P less than 0.05) were decreased. Venous distensibility was improved with captopril (P less than 0.05). All the hemodynamic changes were attenuated by indomethacin (50 mg). Captopril increased circulating bradykinin (P less than 0.05), prostaglandin E2 (P less than 0.05) and 6-keto-prostaglandin F1 alpha (P less than 0.05). Indomethacin did not affect bradykinin level but blocked the increase in prostaglandins. These data suggest that captopril dilates both arterial and venous vessels not only by blocking the renin-angiotensin system but by increasing local or circulating vasodilator prostaglandins.