{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,12]],"date-time":"2023-10-12T05:31:31Z","timestamp":1697088691044},"reference-count":38,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2005,7,13]],"date-time":"2005-07-13T00:00:00Z","timestamp":1121212800000},"content-version":"vor","delay-in-days":12,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2005,7]]},"abstract":"<jats:p><jats:bold>Our aim was to analyse endothelial hypoxic preconditioning after hypoxia\u2013reperfusion (HR). Endothelial functionality was analysed through the vasorelaxation responses to acetylcholine (Ach) and the level of serine<jats:sup>1177<\/jats:sup> phosphorylated endothelial nitric oxide synthase (eNOS) (ser<jats:sup>1177<\/jats:sup>\u2010eNOS) measured by Western blot in <jats:italic>in vitro<\/jats:italic> hypoxic preconditioned (P + HR) isolated rat aortic segments. Relaxation in response to Ach was reduced in phenylephrine\u2010precontracted aortic segments after HR (control: IC<jats:sub>50<\/jats:sub>, 5 \u00b1 2.5 \u00d7 10<jats:sup>\u22128<\/jats:sup> mol l<jats:sup>\u22121<\/jats:sup>; HR: IC<jats:sub>50<\/jats:sub>, 3 \u00b1 1.2 \u00d7 10<jats:sup>\u22127<\/jats:sup> mol l<jats:sup>\u22121<\/jats:sup>; <jats:italic>P<\/jats:italic> &lt; 0.05). Ach\u2010dependent vasodilatation was improved by P + HR. The content of ser<jats:sup>1177<\/jats:sup>\u2010eNOS in the HR segments was 1.5\u2010fold lower than in P + HR. Confocal microscopy showed an increased content of both superoxide anion and peroxynitrite in the vascular wall of HR aortic segments, which it was reduced by P + HR. Geldanamycin (10 \u03bcg ml<jats:sup>\u22121<\/jats:sup>), an agent known to inhibit heat shock protein 90 (hsp90), reduced the level of ser<jats:sup>1177<\/jats:sup>\u2010eNOS in P + HR aortic segments. However in the presence of geldanamycin, endothelial hypoxic preconditioning persisted. We conclude that short periods of hypoxia induced endothelial hypoxic preconditioning that was accompanied by enhanced levels of ser<jats:sup>1177<\/jats:sup>\u2010eNOS in the vascular wall. The fact that endothelial hypoxic preconditioning persisted in the presence of geldanamycin suggests that other molecular mechanisms are involved in the endothelial adaptation to HR injury.<\/jats:bold><\/jats:p>","DOI":"10.1113\/expphysiol.2005.030163","type":"journal-article","created":{"date-parts":[[2005,3,16]],"date-time":"2005-03-16T03:28:34Z","timestamp":1110943714000},"page":"557-569","source":"Crossref","is-referenced-by-count":5,"title":["Endothelial hypoxic preconditioning in rat hypoxic isolated aortic segments"],"prefix":"10.1113","volume":"90","author":[{"given":"Carolina","family":"Carrasco\u2010Mart\u00edn","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sergio","family":"Alonso\u2010Orgaz","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Juan C.","family":"De la 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