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Article: Roles of KATP channels in delayed cardioprotection and intracellular Ca2+ in the rat heart as revealed by κ-opioid receptor stimulation with U50,488H

TitleRoles of KATP channels in delayed cardioprotection and intracellular Ca2+ in the rat heart as revealed by κ-opioid receptor stimulation with U50,488H
Authors
KeywordsKappa-opioid receptor
Preconditioning
ATP-sensitive potassium channel
Intracellular Ca2+
U50,488H
Issue Date2003
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjp
Citation
British Journal of Pharmacology, 2003, v. 140 n. 4, p. 750-758 How to Cite?
AbstractThe effect of preconditioning with U50488 H (UP), a selective kappa-opioid receptor (kappa-OR) agonist, on infarct size and intracellular Ca2+ ([Ca2+]i) in the heart subjected to ischaemic insults were studied and evaluated. U50488 H administered intravenously reduced the infarct size 18-48 h after administration in isolated hearts subjected to regional ischaemia/reperfusion (I/R). The effect was dose dependent. A peak effect was reached at 10 mg x kg-1 U50488 H and at 24 h after administration. The effect of 10 mg x kg-1 U50488 H at 24 h after administration was abolished by nor-binaltorphimine (nor-BNI), a selective kappa-OR antagonist, indicating the effect was kappa-OR mediated. The infarct reducing effect of U50488 H was attenuated when a selective blocker of mitochondrial (5-hydroxydecanoic acid, 5-HD) or sarcolemmal (HRM-1098) ATP-sensitive potassium channel (KATP) was coadministered with U50488 H 24 h before ischaemia or when 5-HD was administered just before ischaemia. U50488 H also attenuated the elevation in [Ca2+]i and reduction in electrically induced [Ca2+]i transient in cardiomyocytes subjected to ischaemic insults. The effects were reversed by blockade of KATP channel, which abolished the protective effect of preconditioning with U50488 H. The results indicated that mitochondrial KATP channel serves as both a trigger and a mediator, while sarcolemmal KATP channel as a trigger only, of delayed cardioprotection of kappa-OR stimulation. The effects of these channels may result from prevention/attenuation of [Ca2+]i overload induced by ischaemic insults.
Persistent Identifierhttp://hdl.handle.net/10722/49309
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChen, Men_HK
dc.contributor.authorZhou, JJen_HK
dc.contributor.authorKam, KWLen_HK
dc.contributor.authorQi, JSen_HK
dc.contributor.authorYan, WYen_HK
dc.contributor.authorWu, Sen_HK
dc.contributor.authorWong, TMen_HK
dc.date.accessioned2008-06-12T06:39:02Z-
dc.date.available2008-06-12T06:39:02Z-
dc.date.issued2003en_HK
dc.identifier.citationBritish Journal of Pharmacology, 2003, v. 140 n. 4, p. 750-758en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49309-
dc.description.abstractThe effect of preconditioning with U50488 H (UP), a selective kappa-opioid receptor (kappa-OR) agonist, on infarct size and intracellular Ca2+ ([Ca2+]i) in the heart subjected to ischaemic insults were studied and evaluated. U50488 H administered intravenously reduced the infarct size 18-48 h after administration in isolated hearts subjected to regional ischaemia/reperfusion (I/R). The effect was dose dependent. A peak effect was reached at 10 mg x kg-1 U50488 H and at 24 h after administration. The effect of 10 mg x kg-1 U50488 H at 24 h after administration was abolished by nor-binaltorphimine (nor-BNI), a selective kappa-OR antagonist, indicating the effect was kappa-OR mediated. The infarct reducing effect of U50488 H was attenuated when a selective blocker of mitochondrial (5-hydroxydecanoic acid, 5-HD) or sarcolemmal (HRM-1098) ATP-sensitive potassium channel (KATP) was coadministered with U50488 H 24 h before ischaemia or when 5-HD was administered just before ischaemia. U50488 H also attenuated the elevation in [Ca2+]i and reduction in electrically induced [Ca2+]i transient in cardiomyocytes subjected to ischaemic insults. The effects were reversed by blockade of KATP channel, which abolished the protective effect of preconditioning with U50488 H. The results indicated that mitochondrial KATP channel serves as both a trigger and a mediator, while sarcolemmal KATP channel as a trigger only, of delayed cardioprotection of kappa-OR stimulation. The effects of these channels may result from prevention/attenuation of [Ca2+]i overload induced by ischaemic insults.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjpen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectKappa-opioid receptoren_HK
dc.subjectPreconditioningen_HK
dc.subjectATP-sensitive potassium channelen_HK
dc.subjectIntracellular Ca2+en_HK
dc.subjectU50,488Hen_HK
dc.titleRoles of KATP channels in delayed cardioprotection and intracellular Ca2+ in the rat heart as revealed by κ-opioid receptor stimulation with U50,488Hen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-1188&volume=140&issue=4&spage=750&epage=758&date=2003&atitle=Roles+of+KATP+channels+in+delayed+cardioprotection+and+intracellular+Ca2++in+the+rat+heart+as+revealed+by+κ-opioid+receptor+stimulation+with+U50,488Hen_HK
dc.identifier.emailChen, M: chenmai@hotmail.comen_HK
dc.identifier.emailKam, KWL: kam_wan_lung@hotmail.comen_HK
dc.identifier.emailYan, WY: yanyi@e-garfield.comen_HK
dc.identifier.emailWu, S: swua@hkucc.hku.hken_HK
dc.identifier.emailWong, TM: wongtakm@hkucc.hku.hken_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1038/sj.bjp.0705475en_HK
dc.identifier.pmid14534156en_HK
dc.identifier.pmcidPMC1574065en_HK
dc.identifier.scopuseid_2-s2.0-0242660884-
dc.identifier.isiWOS:000186240600020-

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