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dc.contributor.authorHeadrick, Johnen_US
dc.contributor.authorGauthier, NS.en_US
dc.contributor.authorMatherne, GP.en_US
dc.description.abstractWe studied the role of mitochondrial ATP-sensitive K+(KATP) channels in modifying functional responses to 20 min global ischemia and 30 min reperfusion in wild-type mouse hearts and in hearts with ~250-fold overexpression of functionally coupled A1-adenosine receptors (A1ARs). In wild-type hearts, time to onset of contracture (TOC) was 303 ᠲ4 s, with a peak contracture of 89 ᠵ mmHg. Diastolic pressure remained elevated at 52 ᠶ mmHg after reperfusion, and developed pressure recovered to 40 ᠶ% of preischemia. A1AR overexpression markedly prolonged TOC to 517 ᠸ4 s, reduced contracture to 64 ᠶ mmHg, and improved recovery of diastolic (to 9 ᠴ mmHg) and developed pressure (to 82 ᠸ%). 5-Hydroxydecanoate (5-HD; 100 卩, a mitochondrial KATPblocker, did not alter ischemic contracture in wild-type hearts, but increased diastolic pressure to 69 ᠸ mmHg and reduced developed pressure to 10 ᠵ% during reperfusion. In transgenic hearts, 5-HD reduced TOC to 348 ᠱ8 s, increased postischemic contracture to 53 ᠴ mmHg, and reduced recovery of developed pressure to 22 ᠴ%. In summary, these data are the first to demonstrate that endogenous activation of KATP channels improves tolerance to ischemia-reperfusion in murine myocardium. This functional protection occurs without modification of ischemic contracture. The data also support a role for mitochondrial KATP channel activation in the pronounced cardioprotection afforded by overexpression of myocardial A1ARs.en_US
dc.publisherAmerican Physiological Societyen_US
dc.relation.ispartofjournalAmerican Journal of Physiology: Heart and Circulatory Physiologyen_US
dc.titleCardioprotection by KATP channels in wild-type hearts and hearts overexpressing A1 adenosine receptorsen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.facultyGriffith Health, School of Medical Scienceen_US
gro.rights.copyrightSelf-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author[s] for more information.en_US
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