Role of Vascular Nitric Oxide in Experimental Liver Cirrhosis

Author(s): Noemi M. Atucha, F. Javi A. Nadal, David Iyu, Antonia Alcaraz, Alicia Rodriguez-Barbero, M. Clara Ortiz, Jose Miguel Lopez-Novoa, Joaquin Garcia-Estan

Journal Name: Current Vascular Pharmacology

Volume 3 , Issue 1 , 2005

Become EABM
Become Reviewer

Abstract:

One of the most important features of liver cirrhosis is the splanchnic and systemic arterial vasodilation, related to an increase in vascular capacity and an active vasodilation. This arterial vasodilation seems to be the consequence of the excessive generation of vasodilating substances, which also contributes to a lower than normal pressor response to circulating nervous or humoral substances. The following review analyzes the mechanisms responsible for the vascular hyporesponse to vasoconstrictors observed in the experimental models of liver cirrhosis. It has become increasingly clear that, among the great variety of substances studied, nitric oxide (NO) seems to be one of the main contributors to this vascular alteration, since elimination of the endothelium or inhibition of its synthesis corrects it. The mechanism by which NO interferes with the contractile apparatus in smooth muscle cells seems to be related to a direct effect on calcium entry from the extracellular space and release from the internal stores.

Keywords: endothelium, smooth muscle cells, nitric oxide, liver cirrhosis, vasoconstrictors, vasodilation, portal hypertension

open access plus

Rights & PermissionsPrintExport Cite as

Article Details

VOLUME: 3
ISSUE: 1
Year: 2005
Page: [81 - 85]
Pages: 5
DOI: 10.2174/1570161052773889

Article Metrics

PDF: 13