Infusion of indomethacin into anesthetized, salt-depleted dogs cuased an increase in mean arterial blood pressure (MABP), and decreases in heart rate (HR), urine flow rate (V), renal plasma flow (RPF), and renin secretion rate. MABP was 112.1 +/-5.4 mm Hg during control periods and was 147.7 +/- 5.6 mm Hg (P less than 0.005) 80 minutes after the infusion of indomethacin. V was 0.38 +/- 0.06 ml/min during control periods and was 0.08 +/- 0.01 ml/min (P less than 0.005) 80 minutes after the infusion of indomethacin. RPF was 126.3 +/- 13.3 ml/min and 41.5 +/- 7.5 ml/min, respectively (P less than 0.005), before and after 80 minutes of infusion. Renin secretion rate decreased from 1,194.1 +/- 353.9 U/min during control periods to reach 384.0 +/- 125.8 U/min (P less than 0.025) by 80 minutes of infusion of indomethacin. Subsequent infusion of prostaglandin E2 (PGE2) into the renal artery for 80 minutes caused increases of V to 0.53 +/- 0.13 ml/min (P less than 0.01), of RPF to 102.4 +/- 23.1 ml/min (P less than 0.01), and of renin secretion rate to 2,582.6 +/- 786.4 U/min (P less than 0.005). The decrease in renin secretion rate during the infusion of indomethacin persisted when renal perfusion pressure (RPP) was maintained relatively constant before and during the infusion of indomethacin. Furthermore, we found that infusion of prostaglandin E1 (PGE1) into the kidney gave the same pattern of response as PGE2. The data suggest that PGE1 and PGE2 play a role in the control of renin secretion.