{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T15:25:50Z","timestamp":1791473150984,"version":"4.3.4"},"reference-count":27,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2005,4,22]],"date-time":"2005-04-22T00:00:00Z","timestamp":1114128000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Acta Physiologica Scandinavica"],"published-print":{"date-parts":[[2005,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:bold>Objective:\u2002<\/jats:bold> Hypoxia induces coronary artery dilation, but the responsible mechanism is largely unknown. Many stimuli induce arterial smooth muscle relaxation by reducing ser<jats:sup>19<\/jats:sup>\u2010myosin regulatory light chain (MLC) phosphorylation. Other stimuli can induce smooth muscle relaxation without reductions in ser<jats:sup>19<\/jats:sup>\u2010MLC phosphorylation. This form of relaxation has been termed force suppression and appears to be associated with heat shock protein 20 (HSP20) phosphorylation on ser<jats:sup>16<\/jats:sup>. We investigated whether hypoxia\u2010induced sustained dilation in swine coronary arteries was promoted without ser<jats:sup>19<\/jats:sup>\u2010MLC dephosphorylation and associated with ser<jats:sup>16<\/jats:sup>\u2010HSP20 phosphorylation. Nitroglycerin vasodilation served as control.<\/jats:p><jats:p><jats:bold>Methods:\u2002<\/jats:bold> In a pressure myograph, the tunica media of intact pre\u2010contracted (PGF<jats:sub>2<jats:italic>\u03b1<\/jats:italic><\/jats:sub>; 10<jats:sup>\u22125<\/jats:sup>\u2003<jats:sc>m<\/jats:sc>) porcine coronary artery segments were cannulated using a microdialysis catheter. Diameter responses and interstitial lactate\/pyruvate ratios were studied during 90\u2003min hypoxia, hypoxia\u2003+\u2003reoxygenation (60\u2003min), nitroglycerin (100\u2003<jats:italic>\u03bc<\/jats:italic><jats:sc>m<\/jats:sc>, 90\u2003min), and nitroglycerin\u2003+\u2003wash\u2010out (60\u2003min). The arterial segments were snap\u2010frozen and analysed for ser<jats:sup>16<\/jats:sup>\u2010HSP20 phosphorylation and ser<jats:sup>19<\/jats:sup>\u2010MLC phosphorylation.<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> The normalized diameter responses to hypoxia (6.1\u2003\u00b1\u20034.3%) and nitroglycerin (12.6\u2003\u00b1\u20031.6%) were both significantly greater than normoxic control arteries (\u221210.5\u2003\u00b1\u20031.8%, <jats:sc>anova<\/jats:sc>, <jats:italic>P<\/jats:italic>\u2003&lt;\u20030.05). Ser<jats:sup>16<\/jats:sup>\u2010HSP20 phosphorylation was increased with hypoxia and nitroglycerin treatment and ser<jats:sup>16<\/jats:sup>\u2010HSP20 phosphorylation correlated with changes in diameters (<jats:italic>n<\/jats:italic>\u2003=\u200329, <jats:italic>r<\/jats:italic><jats:sup>2<\/jats:sup>\u2003=\u20030.64, <jats:italic>P<\/jats:italic>\u2003&lt;\u20030.001). Ser<jats:sup>19<\/jats:sup>\u2010MLC phosphorylation was not significantly altered by hypoxia. The lactate\/pyruvate ratio was significantly increased in hypoxic arteries but did not correlate with diameters or ser<jats:sup>16<\/jats:sup>\u2010HSP20 phosphorylation.<\/jats:p><jats:p><jats:bold>Conclusion:\u2002<\/jats:bold> Ser<jats:sup>16<\/jats:sup>\u2010HSP20 phosphorylation is a potential regulator of hypoxia\u2010induced dilation in coronary arteries.<\/jats:p>","DOI":"10.1111\/j.1365-201x.2005.01426.x","type":"journal-article","created":{"date-parts":[[2005,4,23]],"date-time":"2005-04-23T00:36:59Z","timestamp":1114216619000},"page":"37-44","source":"Crossref","is-referenced-by-count":11,"title":["HSP20 phosphorylation and interstitial metabolites in hypoxia\u2010induced dilation of swine coronary arteries"],"prefix":"10.1111","volume":"184","author":[{"given":"O.","family":"Fr\u00f8bert","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. 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