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Articles in PresS, published online ahead of print April 24, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00391.2001
Submitted on September 7, 2001
Accepted on April 22, 2002
1 Department of Pharmacology and Human Physiology, University of Bari, Bari, Italy
2 Lab.Pharmacologie et Physico-Chimie des Interactions Cellulaires et Moleculaires, UMR CNRS 7034, Illkirch Cedex, France
* To whom correspondence should be addressed. E-mail: chieppa{at}farmacol.uniba.it.
Expression of constitutive and inducible cyclooxygenase (COX-1, COX-2) and the role of prostanoids were investigated in aorta and mesenteric vascular bed (MVB) from portal vein-ligated rat (PVL) as a model of portal hypertension. Functional experiments were carried out in MVB from PVL and sham-operated rats in absence or presence of the non-selective COX-inhibitor indomethacin, or the selective inhibitors of COX-1, SC-560, or COX-2, NS-398. Western blot of COX-1 and COX-2 proteins were evaluated in aorta and MVB, PGI2 productions by enzyme-immunoassay of 6-ketoPGF1 
was evaluated in aorta. In presence of functional endothelium, decreased contraction to norepinephrine (NE) and increased vasodilatation to acethylcholine (ACh) were observed in MVB from PVL. Exposure of MVB to indomethacin, SC-560 or NS-398 reversed the hyporeactivity to NE and the increased endothelial vasodilatation to ACh in PVL, NS-398 being more potent than other two inhibitors. Upregulation of COX-1 and COX-2 expressions were detected in aorta and MVB from PVL portal hypertensive rats and increased production of 6-ketoPGF1 was observed in aorta from portal hypertensive rats. These results suggest that generation of endothelial vasodilator prostanoids, from COX-1 and COX-2 isoforms, accounts for the increased mesenteric blood flow in portal hypertension.
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