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Updated: Oct 9, 2026
Two-photon Imaging of Intracellular Ca2+ Handling and Nitric Oxide Production in Endothelial and Smooth Muscle Cells of an Isolated Rat Aorta
Published on: June 10, 2015
Endothelial, but not the inducible, nitric oxide synthase is detectable in normal and portal hypertensive rats
Michael Martin Stumm1, Daniel D'Orazio, Lazar Trajan Sumanovski
1Department of Research, University Hospital Basel, 4031-Basel, Switzerland. michael.stumm@unibas.ch
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.
