Angiotensin-induced sodium excretion patterns in cirrhosis: role of renal prostaglandins.

Changes in renal hemodynamics and sodium excretion induced by an angiotensin II (AII) infusion were correlated with urinary prostaglandin E2 (PGE2) excretion in 15 patients with cirrhosis and ascites. All induced natriuretic responses in 47% and antinatriuretic responses in 53% of the patients. Natriuresis was accompanied by an increase; antinatriuresis by a decrease in PGE2 excretion. Although there was no change in GFR (CIn), renal blood flow (CPAH) decreased. Patients were clinically indistinguishable. Antinatriuretic responders tended, however, to have higher baseline PGE2 excretion rates, were more sensitive to effects of prostaglandin blockade, and were less sensitive to the pressor effect of AII. Following partial inhibition of renal prostaglandin synthesis by indomethacin, AII-induced natriuretic responses were accentuated. GFR, RBF, and urine flow rate markedly decreased in both groups. There was no difference in pressor sensitivity to AII following prostaglandin synthesis blockade. We conclude that in patients with hepatic cirrhosis, the sodium excretion pattern induced by an exogenous AII challenge may depend on the prior state of intrarenal prostaglandin activity. Our findings also support the hypothesis that renal hemodynamic parameters in patients with cirrhosis and ascites are crucially dependent on renal prostaglandins.