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Article: The K(Ca) channel as a trigger for the cardioprotection induced by kappa-opioid receptor stimulation –- its relationship with protein kinase C

TitleThe K(Ca) channel as a trigger for the cardioprotection induced by kappa-opioid receptor stimulation –- its relationship with protein kinase C
Authors
KeywordsKappa opioid receptor
Ca2+-activated potassium channel
Ischaemia and reperfusion
Metabolic inhibition and anoxia
Issue Date2005
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjp
Citation
British Journal of Pharmacology, 2005, v. 145 n. 7, p. 984-991 How to Cite?
AbstractWe first determined whether the cardioprotection resulting from kappa opioid receptor (kappa-OR) stimulation was blocked by the K(Ca) channel inhibitor, paxilline (Pax), administered before or during ischaemic insults in vitro. In isolated rat hearts, 30 min of ischaemia and 120 min of reperfusion induced infarction and increased lactate dehydrogenase (LDH) release. In isolated ventricular myocytes subjected to 5 min of metabolic inhibition and anoxia followed by 10 min of reperfusion, the percentage of live cells and the amplitude of the electrically induced intracellular Ca(2+) ([Ca(2+)](i)) transient decreased, while diastolic [Ca(2+)](i) increased. Pretreatment with 10 microM U50,488H, a kappa-OR agonist, attenuated the undesirable effects of ischaemic insults in both preparations. The beneficial effects of kappa-OR stimulation, that were abolished by 5 microM nor-BNI, a kappa-OR antagonist, were also abolished by 1 microM Pax administered before ischaemic insults or 20 microM atractyloside, an opener of the mitochondrial permeability transition pore. Activation of protein kinase C (PKC) with 0.1 microM phorbol 12-myristate 13-acetate decreased the infarct size and LDH release in isolated rat hearts subjected to ischaemia/reperfusion, and these effects were abolished by blockade of PKC with its inhibitors, 10 microM GF109203X or 5 microM chelerythrine, and more importantly by 1 microM Pax. On the other hand, the cardioprotective effects of opening the K(Ca) channel with 10 microM NS1619 were not altered by either PKC inhibitor. In conclusion, the high-conductance K(Ca) channel triggers cardioprotection induced by kappa-OR stimulation that involves inhibition of MPTP opening. The K(Ca) channel is located downstream of PKC.
Persistent Identifierhttp://hdl.handle.net/10722/49289
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCao, Cen_HK
dc.contributor.authorChen, Men_HK
dc.contributor.authorWong, TMen_HK
dc.date.accessioned2008-06-12T06:38:37Z-
dc.date.available2008-06-12T06:38:37Z-
dc.date.issued2005en_HK
dc.identifier.citationBritish Journal of Pharmacology, 2005, v. 145 n. 7, p. 984-991en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49289-
dc.description.abstractWe first determined whether the cardioprotection resulting from kappa opioid receptor (kappa-OR) stimulation was blocked by the K(Ca) channel inhibitor, paxilline (Pax), administered before or during ischaemic insults in vitro. In isolated rat hearts, 30 min of ischaemia and 120 min of reperfusion induced infarction and increased lactate dehydrogenase (LDH) release. In isolated ventricular myocytes subjected to 5 min of metabolic inhibition and anoxia followed by 10 min of reperfusion, the percentage of live cells and the amplitude of the electrically induced intracellular Ca(2+) ([Ca(2+)](i)) transient decreased, while diastolic [Ca(2+)](i) increased. Pretreatment with 10 microM U50,488H, a kappa-OR agonist, attenuated the undesirable effects of ischaemic insults in both preparations. The beneficial effects of kappa-OR stimulation, that were abolished by 5 microM nor-BNI, a kappa-OR antagonist, were also abolished by 1 microM Pax administered before ischaemic insults or 20 microM atractyloside, an opener of the mitochondrial permeability transition pore. Activation of protein kinase C (PKC) with 0.1 microM phorbol 12-myristate 13-acetate decreased the infarct size and LDH release in isolated rat hearts subjected to ischaemia/reperfusion, and these effects were abolished by blockade of PKC with its inhibitors, 10 microM GF109203X or 5 microM chelerythrine, and more importantly by 1 microM Pax. On the other hand, the cardioprotective effects of opening the K(Ca) channel with 10 microM NS1619 were not altered by either PKC inhibitor. In conclusion, the high-conductance K(Ca) channel triggers cardioprotection induced by kappa-OR stimulation that involves inhibition of MPTP opening. The K(Ca) channel is located downstream of PKC.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.subjectCa2+-activated potassium channelen_HK
dc.subjectIschaemia and reperfusionen_HK
dc.subjectMetabolic inhibition and anoxiaen_HK
dc.titleThe K(Ca) channel as a trigger for the cardioprotection induced by kappa-opioid receptor stimulation –- its relationship with protein kinase Cen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-1188&volume=145&issue=7&spage=984&epage=991&date=2005&atitle=The+K(Ca)+channel+as+a+trigger+for+the+cardioprotection+induced+by+kappa-opioid+receptor+stimulation+–-+its+relationship+with+protein+kinase+Cen_HK
dc.identifier.emailCao, C: caochunmei@hotmail.comen_HK
dc.identifier.emailChen, M: chenmai@hotmail.comen_HK
dc.identifier.emailWong, TM: wongtakm@hkucc.hku.hken_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1038/sj.bjp.0706268en_HK
dc.identifier.pmid15912131-
dc.identifier.pmcidPMC1576218en_HK
dc.identifier.scopuseid_2-s2.0-23744437437-
dc.identifier.isiWOS:000231252100016-
dc.identifier.citeulike2463008-

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