Deletion of inducible nitric oxide synthase decreases mesenteric vascular responsiveness in portal hypertensive mice
Abstract
The effects of pre-hepatic portal hypertension were examined on the responsiveness of aorta and mesenteric artery from wild-type, inducible nitric oxide synthase knockout (iNOS-KO) and endothelial nitric oxide synthase knockout (eNOS-KO) mice. Mice were sham-operated or made portal hypertensive by creating a calibrated portal vein stenosis. Acetylcholine produced marked relaxations in phenylephrine (10 microM) contracted aorta and mesenteric artery from wild-type and iNOS-KO, both sham and portal hypertensive, but relaxations were abolished in vessels from eNOS-KO mice. There were no significant differences between sham and portal hypertensive animals within groups in the effects of acetylcholine. The potency of KCl was significantly increased in aorta and mesenteric artery from eNOS-KO mice. The maximum contraction to the alpha(1)-adrenoceptor agonist phenylephrine was significantly increased in aorta from eNOS-KO, as compared with wild-type mice. There were no significant differences between sham and portal hypertensive animals within each group in contractions of aorta to KCl or phenylephrine. However, in mesenteric artery, although portal hypertension did not change responsiveness in wild-type or eNOS-KO as compared to sham...Continue Reading
References
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