Deletion of inducible nitric oxide synthase decreases mesenteric vascular responsiveness in portal hypertensive mice

European Journal of Pharmacology
Sotiria BexisJ R Docherty

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

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Citations

Jan 9, 2013·European Journal of Clinical Investigation·Chiao-Lin ChuangShou-Dong Lee
Oct 20, 2006·Vascular Pharmacology·C L M SilvaF Noël
Sep 5, 2006·European Journal of Pharmaceutical Sciences : Official Journal of the European Federation for Pharmaceutical Sciences·Ale LaukevicieneThomas Herdegen
May 10, 2005·European Journal of Pharmacology·Khalid Al ZubairJames R Docherty

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