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.

The purpose of the study was to investigate the effects on urine flow and osmolar excretion of arachidonic acid (C20:4) infused in the renal artery of anaesthetized rats under conditions in which indomethacin previously was found to reduce urine flow and to prevent the development of a moderate saline diuresis. C20:4 caused a reversible increase in the urinary excretion rates of PGE2 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 anaesthesia. 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. The main conclusions are that endogenous renal PG's have a diuretic effect in the amytal anaesthetized rat, while an effect on osmolar excretion rate is apparent only under hydropenic conditions. 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 prostaglandins.