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Am J Physiol Gastrointest Liver Physiol 283: G587-G594, 2002. First published April 24, 2002; doi:10.1152/ajpgi.00391.2001
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Vol. 283, Issue 3, G587-G594, September 2002

Endothelial COX-1 and -2 differentially affect reactivity of MVB in portal hypertensive rats

M. A. Potenza1, O. A. Botrugno1, M. A. De Salvia1, G. Lerro1, C. Nacci1, F. L. Marasciulo1, R. Andriantsitohaina2, and D. Mitolo-Chieppa1

1 Section of Pharmacology, Department of Pharmacology and Human Physiology, Medical School, University of Bari, 70124 Bari, Italy; and 2 Faculté de Pharmacie, Laboratoire de Pharmacologie et Physicochimie des Interactions Cellulaires et Moléculaires, Unité Mixte de Recherche Centre National de la Recherche Scientifique, 67401 Illkirch Cedex, France

Expression of constitutive and inducible cyclooxygenase (COX-1 and COX-2, respectively) and the role of prostanoids were investigated in the aorta and mesenteric vascular bed (MVB) from the 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 the absence or presence of the nonselective COX inhibitor indomethacin or the selective inhibitors of COX-1 (SC-560) or COX-2 (NS-398). Western blots of COX-1 and COX-2 proteins were evaluated in aorta and MVB, and PGI2 production by enzyme immunoassay of 6-keto-PGF1alpha was evaluated in the aorta. In the presence of functional endothelium, decreased contraction to norepinephrine (NE) and increased vasodilatation to 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, with NS-398 being more potent than the other two inhibitors. Upregulation of COX-1 and COX-2 expressions was detected in aorta and MVB from PVL portal hypertensive rats, and increased production of 6-keto-PGF1alpha 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.

vasodilator prostanoids; vascular hyporeactivity; resistance vessels; cyclooxygenase; mesenteric vascular bed; portal vein-ligated


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