Participation of the prostaglandin system in furosemide-induced changes of renal function in anesthetized rats.
The possible mediation of the endogenous prostaglandin and kallikrein-kinin systems of changes in renal function induced by furosemide was studied in anesthetized rats. Increasing doses of furosemide infusion (0.03, 0.1, and 0.3 mg/kg/min) caused dose-related diuresis, natriuresis, kaliuresis, and decreased renal blood flow and urinary osmolality without any significant changes in mean arterial blood pressure. Pretreatment with the prostaglandin synthetase inhibitor indomethacin resulted in marked reduction of the water and sodium excretion induced by furosemide. It also blunted renal vasoconstriction and renin release by furosemide, but the glomerular filtration rate was not affected. Pretreatment with aprotinin, a kallikrein inhibitor, failed to affect the renal response to furosemide. The results indicate that the renal prostaglandin system, but not the kallikrein-kinin system, participates in the effect of furosemide on renal functions mainly through electrolyte transport inhibition in the renal tubule.
D000818:Animals; D007611:Aprotinin / Q000494:pharmacology; D004231:Diuresis / Q000187:drug effects; D005665:Furosemide / Q000494:pharmacology*; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000502:physiology*; D008297:Male; D011453:Prostaglandins / Q000502:physiology*; D051381:Rats; D011921:Rats, Inbred WKY
D011453:Prostaglandins; D005665:Furosemide; D007611:Aprotinin; D007213:Indomethacin