Endothelial, but not the inducible, nitric oxide synthase is detectable in normal and portal hypertensive rats

: 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 di...

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Published in:Liver (Copenhagen) 2002-12, Vol.22 (6), p.441-450
Main Authors: Stumm, Michael Martin, D'Orazio, Daniel, Sumanovski, Lazar Trajan, Martin, Pierre-Yves, Reichen, Juerg, Sieber, Cornel Christian
Format: Article
Language:English
Subjects:
Animals
Blotting, Western
cirrhosis
Disease Models, Animal
Fluorescent Antibody Technique, Indirect
Hypertension, Portal - enzymology
Hypertension, Portal - etiology
immunoblotting
Immunoenzyme Techniques
immunohistochemistry
Liver Cirrhosis, Experimental - complications
Liver Cirrhosis, Experimental - enzymology
Macrophages - enzymology
Male
nitric oxide
Nitric Oxide Synthase - biosynthesis
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type III
portal hypertension
Rats
Rats, Sprague-Dawley
Thymus Gland - enzymology
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Summary:: 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.
ISSN:0106-9543
1600-0676
DOI:10.1034/j.1600-0676.2002.01653.x