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Abstract
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 < 0.01) and venous pressure (P < 0.05); forearm blood flow (P < 0.05) and maximum venous volume (P < 0.05) were increased; forearm vascular resistance (P < 0.05) and forearm venous tone (P < 0.05) were decreased. Venous distensibility was improved with captopril (P < 0.05). All the hemodynamic changes were attenuated by indomethacin (50mg). Captopril increased circulating bradykinin (P < 0.05), prostaglandin E2 (P < 0.05) and 6-keto-prostaglandin F1α (P < 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.