{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,7,22]],"date-time":"2024-07-22T18:32:43Z","timestamp":1721673163356},"reference-count":43,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":759,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2007,1]]},"abstract":"<jats:sec><jats:title>Background and purpose:<\/jats:title><jats:p>The present study investigated mechanisms underlying impaired endothelium\u2010dependent vasodilatation elicited by elevating the intraluminal pressure in rat mesenteric small arteries.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental approach:<\/jats:title><jats:p>Arterial segments (internal diameter 316\u00b12\u2003<jats:italic>\u03bc<\/jats:italic>m, n=86) were mounted in a pressure myograph. The effect of elevating pressure from 50 to 120\u2003mmHg for 1\u2003h before resetting it to 50\u2003mmHg was studied on endothelium\u2010dependent vasodilatation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key results:<\/jats:title><jats:p>In arteries constricted with U46619 in the presence of indomethacin, shear stress generated by flow, evoked vasodilatation that was abolished by an inhibitor of nitric oxide (NO) synthase, asymmetric dimethylarginine (1\u2003mM), whereas acetylcholine\u2010induced vasodilatation was unchanged. After elevation of intraluminal pressure for 1\u2003h and then resetting it to 50\u2003mmHg, vasodilatation induced by shear stress and the NO donor, S\u2010nitrosopenicillamine was inhibited, while vasodilatation induced by a guanylyl cyclase activator, BAY 412272, and acetylcholine was unaltered. Superoxide levels sensitive to polyethylene glycol superoxide dismutase were increased in segments exposed to elevated pressure. A superoxide scavenger, tempol (300\u2003<jats:italic>\u03bc<\/jats:italic>M), a general endothelin receptor antagonist, SB 217242 and the selective ET<jats:sub>A<\/jats:sub> receptor antagonist, BQ 123 preserved shear stress\u2010evoked vasodilatation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and Implications:<\/jats:title><jats:p>The present study shows that transient exposure to an elevated intraluminal pressure selectively inhibits flow\u2010evoked NO\u2010mediated vasodilatation, probably through activation of endothelin receptors and increased formation of superoxide. In contrast, elevation of pressure did not affect the acetylcholine\u2010evoked endothelium\u2010derived hyperpolarizing factor type vasodilatation in mesenteric small arteries.<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2007) <jats:bold>150<\/jats:bold>, 80\u201387. doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0706965\">10.1038\/sj.bjp.0706965<\/jats:ext-link><\/jats:p><\/jats:sec>","DOI":"10.1038\/sj.bjp.0706965","type":"journal-article","created":{"date-parts":[[2006,11,27]],"date-time":"2006-11-27T12:44:16Z","timestamp":1164631456000},"page":"80-87","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Elevated pressure selectively blunts flow\u2010evoked vasodilatation in rat mesenteric small arteries"],"prefix":"10.1111","volume":"150","author":[{"given":"F 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