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- W815110 abstract "NO-independent, endothelium-derived mediators are important regulators of vascular tone. The goal of this study was to determine how arachidonic acid (AA) metabolism through cyclooxygenase-1 (COX-1) and COX-2 isoforms regulates vasoreactivity in mouse mesenteric arteries, in the absence of NO activity. Arterial rings were suspended for isometric contraction in the presence of the NO synthase inhibitor, Nω-nitro-L-arginine methyl ester (L-NAME, 1 mM). In arteries contracted with the α1-adrenergic agonist phenylephrine, AA (10 to 300 μM) caused relaxation, which was inhibited by the non-selective COX inhibitor indomethacin (3 μM) or the selective COX-1 inhibitor SC-560 (0. 3 μM). In a similar manner, acetylcholine (0.1 to 100 μM) caused relaxation of phenylephrine-induced contraction which was reduced by indomethacin or SC-560. In contrast, AA-induced relaxation was increased by the selective COX-2 inhibitor celecoxib (1 μM). Celecoxib did not affect relaxation to acetylcholine. After endothelial-denudation, AA (10 to 300 μM) increased phenylephrine-induced contraction and this amplification was inhibited by celecoxib. These results suggest that endothelial COX-1-derived AA metabolites contribute to NO-independent relaxation, whereas COX-2-derived metabolites, which are likely generated by the smooth muscle, counter this dilator activity." @default.
- W815110 created "2016-06-24" @default.
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- W815110 date "2007-04-01" @default.
- W815110 modified "2023-10-13" @default.
- W815110 title "COX‐1 and COX‐2 differentially regulate vascular tone in mouse mesenteric artery" @default.
- W815110 doi "https://doi.org/10.1096/fasebj.21.5.a495-b" @default.
- W815110 hasPublicationYear "2007" @default.
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