NITRIC OXIDE-MEDIATED BETA(2)-ADRENOCEPTOR RELAXATION IS IMPAIRED IN MESENTERIC VEINS FROM PORTAL-HYPERTENSIVE RATS

Background & Aims: beta-Adrenergic relaxation seems to be mediated by nitric oxide, The aim of this study was to evaluate changes induced by portal hypertension in beta 2-adrenergic vasorelaxation, Methods: Iso lated rat mesenteric veins were relaxed by salbutamol, and nerve-media ted vasocontractions were induced by electrical field stimulation, Res ponses were evaluated in the presence of N-G-nitro-L-arginine methyl e ster (L-NAME) or tetrodotoxin. Immunocytochemical techniques were used for localization of neuronal NO synthase. Results: Salbutamol-induced relaxations were decreased in rings from portal-hypertensive animals, L-NAME reduced these relaxations, but its effects were more pronounce d in sham-operated rats. Tetrodotoxin decreased the effect of salbutam ol only in rings from sham-operated animals. Combination of L-NAME and tetrodotoxin did not exert a greater effect, than either of these age nts alone, Veins from portal-hypertensive animals were move sensitive to S-nitroso-N-acetyl penicillamine. L-NAME increased vasocontractions by electrical stimulation only in rings from sham-operated rats. Vein s from portal-hypertensive animals exhibited a specific degeneration o f NO-containing nerve endings, Conclusions: beta(2)-Adrenergic relaxat ion is impaired in mesenteric veins from portal-hypertensive rats, pos sibly as a result of a defective neuronal release of NO.