ROLE OF NITRIC-OXIDE AND PROSTACYCLIN IN THE CONTROL OF RENAL PERFUSION IN EXPERIMENTAL CIRRHOSIS

Nitric oxide (NO) and prostacyclin (PGI(2)) are two important modulato rs of renal function under normal conditions; however, little is known on their contributory role in cirrhosis with ascites, In this study, mean arterial pressure, renal hemodynamics, and sodium excretion were measured in 15 rats with cirrhosis and ascites and 16 control rats, An imals were studied in normal conditions, after inhibiting the synthesi s of NO (N-omega-nitro-L-arginine, 50 mu g . kg(-1). min(-1)) or prost aglandins (lysine acetylsalicylate, 15 mg . kg(-1). min(-1)) and follo wing the concomitant inhibition of both systems, Cirrhotic rats showed increased systemic pressure sensitivity and blunted renal vasoconstri ctor response to nitric oxide inhibition as compared with control rats , As a consequence, the glomerular filtration rate increased in cirrho tic rats but not in control rats. In both groups of animals, NO inhibi tion was associated with significant increased urinary sodium and frac tional sodium excretion, The only significant effect observed after pr ostaglandin biosynthesis inhibition was a decrease in renal plasma now in cirrhotic rats, The concomitant inhibition of both systems reduced renal plasma flow and did not change glomerular filtration rate, with no differences between control and cirrhotic rats. Prostaglandin inhi bition did not prevent the natriuretic effect of the NO inhibitor in b oth groups of animals, These results indicate that in experimental cir rhosis both NO and PGI(2) play an important role in the maintenance of renal perfusion within normal limits.