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 1 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 greater than 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.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology*; D015232:Dinoprostone; D004285:Dogs; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D011392:Proline / Q000031:analogs & derivatives*; D011458:Prostaglandins E / Q000378:metabolism* / Q000502:physiology; D012079:Renal Circulation / Q000187:drug effects*; D012083:Renin / Q000378:metabolism; D014664:Vasodilation / Q000187:drug effects
D011458:Prostaglandins E; D011392:Proline; D002216:Captopril; D012083:Renin; D015232:Dinoprostone; D007213:Indomethacin