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Article: Activation of mitochondrial ATP-sensitive potassium channels delays ischemia-induced cellular uncoupling in rat heart

TitleActivation of mitochondrial ATP-sensitive potassium channels delays ischemia-induced cellular uncoupling in rat heart
Authors
Issue Date2004
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.html
Citation
Acta Pharmacologica Sinica , 2004, v. 25 n. 1, p. 22-28 How to Cite?
AbstractAIM: To test the hypothesis that cellular uncoupling induced by myocardial ischemia is mediated by activation of mitochondrial ATP-sensitive potassium channels (mitoKATP). METHODS: Rat hearts were perfused on a Langendorff apparatus and subjected to 40-min ischemia followed by 30-min reperfusion (I/R). Changes in cellular coupling were monitored by measuring whole-tissue resistance. RESULTS: (1) In hearts subjected to I/R, the onset of uncoupling started at (13.3+/-1.0) min of ischemia; (2) Ischemic preconditioning (IPC) delayed the onset of uncoupling until (22.7+/-1.3) min. Blocking mitoKATP channels with 5-hydroxydecanoate (5-HD) before the IPC abolished the uncoupling delay [(12.6+/-1.6) min]; (3) Calcium preconditioning (CPC) had the same effect as IPC. And this effect was reversed by blocking the mitoKATP channel again. In the CPC group the onset of uncoupling occurred after (20.6+/-1.3) min, and this was canceled by 5-HD [(13.6+/-0.8) min]; (4) In hearts pretreated with the specific mitoKATP channel opener diazoxide before sustained ischemia, the onset was delayed to (18.4+/-1.4) min; (5) 5-HD canceled the protective effects of diazoxide (12.6+/-1.0) min; and both the L-type Ca2+ channel inhibitor verapamil and the free radical scavenger N-(2-mercaptopropionyl)glycine, reduced the extended onset time induced by diazoxide [to (13.3+/-1.8) min and (13.4+/-2.1) min, respectively]. CONCLUSION: IPC and CPC delay the onset of cellular uncoupling induced by acute ischemia in rat heart, and the underlying mechanism involves activation of the mitoKATP channels.
Persistent Identifierhttp://hdl.handle.net/10722/210021
ISSN
2015 Impact Factor: 3.166
2015 SCImago Journal Rankings: 1.161

 

DC FieldValueLanguage
dc.contributor.authorShen, YL-
dc.contributor.authorChen, YY-
dc.contributor.authorWu, XD-
dc.contributor.authorBruce, IC-
dc.contributor.authorXia, Q-
dc.date.accessioned2015-05-20T02:32:30Z-
dc.date.available2015-05-20T02:32:30Z-
dc.date.issued2004-
dc.identifier.citationActa Pharmacologica Sinica , 2004, v. 25 n. 1, p. 22-28-
dc.identifier.issn1671-4083-
dc.identifier.urihttp://hdl.handle.net/10722/210021-
dc.description.abstractAIM: To test the hypothesis that cellular uncoupling induced by myocardial ischemia is mediated by activation of mitochondrial ATP-sensitive potassium channels (mitoKATP). METHODS: Rat hearts were perfused on a Langendorff apparatus and subjected to 40-min ischemia followed by 30-min reperfusion (I/R). Changes in cellular coupling were monitored by measuring whole-tissue resistance. RESULTS: (1) In hearts subjected to I/R, the onset of uncoupling started at (13.3+/-1.0) min of ischemia; (2) Ischemic preconditioning (IPC) delayed the onset of uncoupling until (22.7+/-1.3) min. Blocking mitoKATP channels with 5-hydroxydecanoate (5-HD) before the IPC abolished the uncoupling delay [(12.6+/-1.6) min]; (3) Calcium preconditioning (CPC) had the same effect as IPC. And this effect was reversed by blocking the mitoKATP channel again. In the CPC group the onset of uncoupling occurred after (20.6+/-1.3) min, and this was canceled by 5-HD [(13.6+/-0.8) min]; (4) In hearts pretreated with the specific mitoKATP channel opener diazoxide before sustained ischemia, the onset was delayed to (18.4+/-1.4) min; (5) 5-HD canceled the protective effects of diazoxide (12.6+/-1.0) min; and both the L-type Ca2+ channel inhibitor verapamil and the free radical scavenger N-(2-mercaptopropionyl)glycine, reduced the extended onset time induced by diazoxide [to (13.3+/-1.8) min and (13.4+/-2.1) min, respectively]. CONCLUSION: IPC and CPC delay the onset of cellular uncoupling induced by acute ischemia in rat heart, and the underlying mechanism involves activation of the mitoKATP channels.-
dc.languageeng-
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.html-
dc.relation.ispartofActa Pharmacologica Sinica-
dc.subject.meshAdenosine Triphosphate - metabolism - physiology-
dc.subject.meshIschemic Preconditioning, Myocardial-
dc.subject.meshMitochondria, Heart - metabolism-
dc.subject.meshMyocardial Reperfusion Injury - etiology - metabolism-
dc.subject.meshPotassium Channels - drug effects-
dc.titleActivation of mitochondrial ATP-sensitive potassium channels delays ischemia-induced cellular uncoupling in rat heart-
dc.typeArticle-
dc.identifier.emailBruce, IC: hrmybic@hkucc.hku.hk-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.pmid14704118-
dc.identifier.hkuros81489-
dc.identifier.volume25-
dc.identifier.issue1-
dc.identifier.spage22-
dc.identifier.epage28-
dc.publisher.placeUnited States-

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