NITRIC-OXIDE DOES NOT CONTRIBUTE TO SODIUM RETENTION AND PERIPHERAL VASODILATION INDUCED BY PARTIAL PORTAL-VEIN LIGATION IN RATS

The role of nitric oxide (NO) synthesis in the peripheral vaso-dilatio n and sodium retention that occurs after partial portal vein ligation (PVL) was investigated. Hemodynamic studies in PVL rats with sodium re tention and in sham-operated controls were conducted on the day when P VL rats developed transient and maximal sodium retention. Measurements were obtained before and during two consecutive periods after NO synt hesis inhibition with NG-monomethyl-L-arginine (L-NMMA). Under baselin e conditions, PVL rats with sodium retention were hypotensive, with eq uivalent decreases in total peripheral resistance and glomerular filtr ation rate in comparison to the control group. After L-NMMA, periphera l resistance and arterial pressure increased by similar extent in both groups. As compared with controls, PVL rats with sodium retention rem ained hypotensive and vasodilated. Furthermore, L-NMMA-induced natriur esis was attenuated the PVL group. Additionally, serum and urinary lev els of nitrate and nitrite did not vary before surgery and at the time of sodium retention. These results suggest that in PVL rats (1) vasod ilation is not NO mediated; (2) vasodilation is not a sufficient expla nation for sodium retention, and (3) a sodium-retaining factor acting on the renal tubules is responsible for sodium retention.