Nitric oxide and portal hypertension: Interface of vasoreactivity and angiogenesis

Daniel A. Langer, Vijay Shah

Research output: Contribution to journalArticle

53 Citations (Scopus)

Abstract

Altered NO signaling plays a central role in the pathogenesis of portal hypertension and many of its complications. Intrahepatic NO synthesis and downstream signaling are inhibited at multiple levels promoting vasoconstriction and increased intrahepatic resistance. Within the splanchnic and systemic circulation there is excess NO production resulting in vasodilation, decreased systemic vascular resistance and increased portal inflow. The portal circulation attempts to decompress through collateral vessels where NO is involved in promoting vasodilation, vascular remodeling and angiogenesis. Alterations in NO synthesis and function also contribute to other complications of portal hypertension including hepatic encephalopathy, hepatopulmonary syndrome, cirrhotic cardiomyopathy, portal hypertensive gastropathy and the hepatorenal syndrome. Although advances in organ-specific delivery are needed, targeted modulation of NO pathways holds great promise for therapeutics in portal hypertension.

Original languageEnglish (US)
Pages (from-to)209-216
Number of pages8
JournalJournal of Hepatology
Volume44
Issue number1
DOIs
StatePublished - Jan 2006

Fingerprint

Portal Hypertension
Nitric Oxide
Vasodilation
Hepatopulmonary Syndrome
Splanchnic Circulation
Hepatorenal Syndrome
Hepatic Encephalopathy
Vasoconstriction
Cardiomyopathies
Vascular Resistance
Therapeutics

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Nitric oxide and portal hypertension : Interface of vasoreactivity and angiogenesis. / Langer, Daniel A.; Shah, Vijay.

In: Journal of Hepatology, Vol. 44, No. 1, 01.2006, p. 209-216.

Research output: Contribution to journalArticle

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