The effect of indomethacin on glomerular capillary pressure and pelvic pressure during ureteral obstruction.
The present investigation was undertaken to determine whether elevated glomerular capillary and pelvic pressure resulting from ureteral obstruction could be lowered by injection of indomethacin. In hydropenic rats and rats subjected to saline volume expansion, the mean arterial blood pressure, renal pelvic pressure and proximal tubular free flow and stop-flow pressures were measured during acute ureteral obstruction. Indomethacin was injected intravenously 30 to 45 minutes after obstruction at a renal pelvic pressure of 35 mm. Hg or higher. In the former group of rats the proximal tubular stop-flow pressure decreased by an average of 32 per cent and renal pelvic pressure by 27 per cent on administration of indomethacin, whereas in the volume expanded rats (saline, 2 per cent of body weight) these pressures did not change significantly. These results suggest that the vasodilation consequent to ureteral obstruction in hydropenic animals is caused by prostaglandins release and can be abolished by indomethacin, whereas the vasodilation that results from ureteral obstruction in volume expanded animals may be affected by additional mechanisms.
D000328:Adult; D000818:Animals; D002196:Capillaries / Q000503:physiopathology; D005260:Female; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology*; D007678:Kidney Glomerulus / Q000187:drug effects* / Q000503:physiopathology; D007682:Kidney Pelvis / Q000503:physiopathology*; D011312:Pressure; D051381:Rats; D011919:Rats, Inbred Strains; D012044:Regression Analysis; D014517:Ureteral Obstruction / Q000503:physiopathology*; D014664:Vasodilation / Q000187:drug effects
D007213:Indomethacin