ROLE OF PROSTAGLANDINS ON THE RENAL EFFECTS OF ANGIOTENSIN AND INTERSTITIAL PRESSURE DURING VOLUME EXPANSION

This study was undertaken to determine, in anesthetized dogs, the role of renal prostaglandins (PG) in mediating the natriuretic response to increased renal interstitial hydrostatic pressure (RIHP) during extra cellular volume expansion (ECVE) with isotonic Wine. It was also deter mined if the intrarenal angiotensin Il (ANG II) effects during ECVE ar e potentiated by the inhibition of PG synthesis. ECVE induced similar elevations of RIHP, natriuresis, and fractional lithium excretion in d ogs treated (n = 7) and not treated with a PG synthesis inhibitor (n = 5). In other experimental groups, the effects of the intrarenal maint enance of ANG II levels (n = 6) by infusing captopril and ANG II into the right renal artery were compared with those induced by the simulta neous infusion of captopril, ANG II, and a PG synthesis inhibitor (n = 6). In response to ECVE, renal blood flow and glomerular filtration r ate were similar in both kidneys when ANG II levels were maintained co nstant and were significantly higher in the left kidney when ANG II le vels were maintained constant and PG synthesis was inhibited in the ri ght kidney. However, when compared with the left kidney, the ECVE-indu ced increments of natriuresis and RIHP in the right kidney were reduce d by the same magnitude when intrarenal ANG II was maintained constant with (36 and 53%, respectively) and without (40 and 54%, respectively ) the simultaneous PG synthesis inhibition. Our results indicate that during ECVE, renal PGs do not play an important role in mediating the RIHP-induced increments in natriuresis and decrements in proximal sodi um reabsorption. Furthermore, it is suggested that PG synthesis inhibi tion does not potentiate the antinatriuretic effects of ANG II during ECVE.