A study of the effect of stimulated endogenous prostaglandin synthesis on urine flow, osmolar excretion rate, and renin release in hydropenic and saline loaded, anesthetized rats

Abstract

This study investigated the effects on urine flow and osmolar excretion of arachidonic acid (C20:4) infused into the renal artery of anesthetized rats under conditions in which indomethacin previously reduced urine flow and prevented the development of a moderate saline diuresis. C20:4 caused a reversible increase in the urinary excretion rates of PG[prostaglandin]E2 and PGF2.alpha. both in hydropenic rats and in rats during a saline diuresis. Renal venous plasma concentration of PGE2 increased significantly while the increase in PGF2.alpha. was insignificant. C20:4 infusion was followed by an increase in urine flow and osmolar excretion rate in hydropenic rats, and it augmented urine flow (but not solute excretion) in saline-loaded rats. This latter effect was blunted by indomethacin treatment and inactin anesthesia. Increased endogenous PG-levels were associated with only a modest (insignificant) increase in renin release under the present conditions. Saline loading acutely depressed PGE2 and PGF2.alpha. urinary excretion rates and plasma renin concentration (PRC). The fall in PRC was unaffected by indomethacin. Evidently, endogenous renal PG have a diuretic effect in the amytal anesthetized rat, while an effect on osmolar excretion rate is apparent only under hydropenic conditons. Acute saline loading depresses renal PG-synthesis, but this depression is not the only cause of the fall in PRC following saline loading. The saline diuresis is caused by a mechanism(s) not involving PG.