Persistent natriuretic effect of prostaglandin D₂ in the dog

Prostaglandin D₂ (PGD₂) has been shown to be a potent renal vasodilating agent although its effects on sodium excretion are controversial. In r123w12 =infused an effort to clarify the renal effects of PGD₂, the agent was infusewd into the renal artery of the dog at two different doses: 0.1 and 1.0 μg/kg/min. At the higher dose of PGD₂ (n=9), renal blood flow (RBF) increased from 186 to 426 ml/min and returned to basal level during the recovery period. Sodium excretion (UNaV) increased from 42 to 102 μEq/min during drug infusion and remained elevated during the recovery period (80 μEq/min). Urinary osmolality (Uosm) fell from 947 to 282 mosm/kg H₂O and remained low during the recovery period (452 mosm/kg H₂O). At the lower dose qualitatively similar changes occurred. Thus, both doses of PGD₂ produced marked renal vasodilatation which was reversible when the drug was discontinued. In contrast, urine flow rate and UNaV increased and Uosm decreased during the infusion of the prostaglandin and these effects persisted after RBF had returned to control values. In additional studies, the persistent diuresis and natriuresis was not found to be related to carbonic anhydrase inhibition or persistent renal prostaglandin E production. Papillary plasma flow (PPF) was estimated during the recovery period in five low-dose PGD₂ experiments. There was a small, but consistent increase in PPF when values from the experimental kidney (32.4 ml of blood/100g of papilla/min) were compared with the values of the control kidney (24.4 ml of blood/100 g of papilla/min). Thus PGD₂, in contrast to other vasodilating agents, causes a persistent increase in urinary volume and sodium excretion and a decrease in urinary osmolality that is not due to an increase in total RBF, but is associated with an increased PPF. This effect is not related to carbonic anhydrase inhibition or increased renal PGE production.