Published online Apr 28, 2015. doi: 10.3748/wjg.v21.i16.4817
Peer-review started: September 4, 2014
First decision: October 14, 2014
Revised: November 3, 2014
Accepted: December 5, 2014
Article in press: December 8, 2014
Published online: April 28, 2015
Core tip: Portal hypertension (PHT) is a complication associated with vascular derangements in response to liver disease and fibrosis. Perturbations of nitric oxide (NO) and endothelin-1 are believed to be interrelated and play a key role in PHT vasculopathy. This study investigates the importance of NO biosynthesis in endothelin-1 vasoconstriction hypo-response seen in patients with PHT. PHT was induced in wild type, eNOS-/- and iNOS-/- mice by partial portal vein ligation (PVL) and endothelin-1 contractile response was determined. Endothelin-1 (ET-1) induced contraction was significantly reduced following PVL in all mouse groups. Aberrant ET-1 function associated with PHT is NO independent.