The Effect of Indomethacin on Glomerular Capillary Pressure and Pelvic Pressure During Ureteral Obstruction

Publisher Website
Google Scholar
Abstract
Whether elevated glomerular capillary and pelvic pressure resulting from ureteral obstruction could be lowered by injection of indomethacin was studied. 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 i.v. 30-45 min after obstruction at a renal pelvic pressure of 35 mm Hg. In the former group of rats the proximal tubular stop-flow pressure decreased by an average of 32% and renal pelvic pressure by 27% on administration of indomethacin; in the volume-expanded rats (saline, 2% body weight) these pressures did not change significantly. Apparently, the vasodilation consequent to ureteral obstruction in hydropenic animals is caused by prostaglandin 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.