Endothelial, but Not the Inducible, Nitric Oxide Synthase is Detectable in Normal and Portal Hypertensive Rats

Overview

Journal Liver

Specialty Gastroenterology

Date 2002 Nov 26

PMID 12445168

Citations 7

Authors

Michael Martin Stumm

Daniel DOrazio

Lazar Trajan Sumanovski

Pierre-Yves Martin

Juerg Reichen

Cornel Christian Sieber

Affiliations

Soon will be listed here.

Abstract

Background: Chronic portal hypertension is accompanied by a nitric oxide (NO) dependent vasodilation. Three isoforms of NO producing synthases (NOS) are characterized: neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). Sources of increased NO levels in chronic hypertension is disputed.

Methods: To determine eNOS and iNOS expression in different organs of portal hypertensive and control rats, we divided Sprague-Dawley rats in 6 groups: (1). Partial portal vein ligated rats, (2). Bile duct ligated rats, (3). Carbon tetrachloride treated rats, (4). Sham operated rats, (5). Untreated control rats, and (6). LPS treated rats. Immunohistochemistry (IHC) and immunoblotting (IB) using antibodies against eNOS or iNOS were carried out on samples from thymus, aorta, heart, lung, oesophagus, liver, spleen, kidney, pancreas, small and large intestine.

Results: IHC revealed an even eNOS expression in all groups. Expression of iNOS was restricted to macrophages in organs of LPS treated and the thymus of rats. IB mirrored these results.

Conclusion: In chronic portal hypertension, the main source for NO production depends on eNOS activity.

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