Investigations of the function of the vascular endothelium in portal hypertensive rats

There were no differences between mesenteric arteries from sham or 14-day portal hypertensive (PH) rats in the potency of or maximum endothelium-dependent relaxations (EDR) to acetylcholine. There were no differences between sham-operated and PH rats in the effects of the combination of the nitric oxide synthase inhibitor N-G-monomethyl-L-arginine (100 mu mol/l) and methylene blue (10 mu mol/l) in causing a significant reduction in the EDR to acetylcholine. The degree of portal-systemic shunting, as measured by Co-57-labeled microspheres, was unaffected by acute administration of N-G-monomethyl-L-arginine (50 mg/kg) or methylene blue (5 mg/kg). In conclusion, nitric oxide is the main mediator of EDR in rat mesenteric artery, and no evidence was found for an increased role for endothelial-derived nitric oxide in PH rats.