This study was designed to determine whether the prostaglandins mediate the renal effects of captopril in the conscious sodium-replete dog. In a group of control animals (n = 8), effective renal plasma flow (ERPF) increased from 185 ± 15 to 230 ± 12 ml/min and plasma renin activity (PRA) increased from 0.64 ± 0.15 to 12.9 ± 1.1 ng ANG I·ml-1·h-1 after captopril (10 mg/kg bolus plus 10 μg·kg-1·min-1i.v.) administration. Glomerular filtration rate (GFR) and sodium excretion (UKV) were also increased significantly following captopril treatment, whereas urine volume (V), potassium excretion (UKV), mean arterial pressure (MAP), and heart rate (HR) remained unchanged throughout the experiment. When the same dose of captopril was given to indomethacin-pretreated dogs (5 mg/kg bolus plus 2 μg·kg-1·min-1i.v.), ERPF increased from 170 ± 8 to 265 ± 18 ml/min and PRA increased from 1.2 ± 0.4 to 14.6 ± 3.0 ng ANG I·ml-1·h-11 after the captopril administration. GFR was also increased significantly after captopril, while UNaV, UKV, and V remained unchanged. These data demonstrate that the prostaglandins do not mediate the ability of captopril to increase PRA or effective renal plasma flow in this experimental model. prostaglandins; effective renal blood flow; plasma renin activity; angiotensin II; arachidonic acid Submitted on September 25, 1981 Accepted on June 25, 1982