CONSTITUTIVE NITRIC-OXIDE MODULATES THE INJURIOUS ACTIONS OF VASOPRESSIN ON RAT INTESTINAL MICROCIRCULATION IN ACUTE ENDOTOXEMIA

The administration of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 5 mg/kg s.c.) concurrently with Escherichia coli endotoxin (3 mg/kg i.v.) increased vascular permeability and caused mucosal damage in the rat intestine 1 h later. The vasopressin V-1 receptor antagonist, [Mca(1),Tyr(Me)(2),Arg(8)]vasopressin (0.01-0.2 mu g/kg s.c., 15 min before endotoxin) dose-dependently reduced this damage. These results suggest a beneficial role of NO, counteracting the injurious vascular actions of endogenous vasopressin, in maintaining intestinal mucosal integrity in acute endotoxaemic states.