Renal PGE₂ release may not be responsible for captopril-induced renal effects in anesthetized dogs

We studied the possible role of renal prostaglandins (PGs) in captopril-induced hypotension, renal vasodilation, and increased renin secretion using anesthetized dogs. An intravenous injection of I mg/kg captopril significantly decreased blood pressure, increased renal blood flow, and raised the renin secretion rate (RSR). These effects of captopril were similar in indomethacin-pretreated (5 mg/kg, i.v.) and in untreated dogs. Captopril administration did not significantly affect the renal PGE₂ secretion rate (p > 0.10). These results suggest that under our experimental conditions, captopril-induced hypotension, renal vasodilation, and increased RSR may not be due to renal PGE₂ release. This does not rule out the possibility that these effects of captopril may be mediated by alterations in the level of circulating bradykinin.