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Article: Effects of pharmacological preconditioning with U50488H on calcium homeostasis in rat ventricular myocytes subjected to metabolic inhibition and anoxia

TitleEffects of pharmacological preconditioning with U50488H on calcium homeostasis in rat ventricular myocytes subjected to metabolic inhibition and anoxia
Authors
KeywordsAnoxia
Metabolic inhibition
Ca2+ homeostasis
Ventricular myocyte
Ca2+ spark
Issue Date2002
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjp
Citation
British Journal of Pharmacology, 2002, v. 137 n. 6, p. 739-748 How to Cite?
Abstract1. The effects of pharmacological preconditioning with U50488H (U(50)), a selective kappa-opioid receptor agonist, on Ca(2+) homeostasis in rat ventricular myocytes subjected for 9 min to metabolic inhibition (MI) and anoxia (A), consequences of ischaemia, were studied and compared with those of preconditioning with brief periods of MI/A. 2. Precondition with 30 micro M of U(50) for three cycles of 1 min each cycle separated by 3 min of recovery (UP) significantly increased the percentage of non-blue cells following MI/A. The effect of UP is the same as that of preconditioning with an inhibitor of glycolysis and an oxygen scavenger for three 1-min cycles separated by three-minute recovery (MI/AP). The results indicate that like MI/AP, UP also confers cardioprotection. 3. MI/A increased intracellular Ca(2+) ([Ca(2+)](i)) and reduced the amplitude of caffeine-induced [Ca(2+)](i) transients, an indication of Ca(2+) content in the sarcoplasmic reticulum (SR). MI/A also reduced the electrically-induced [Ca(2+)](i) transient, that indicates Ca(2+)-release during excitation-contraction coupling, and Ca(2+) sparks in unstimulated myocytes, that indicates spontaneous Ca(2+)-release from SR. It also prolonged the decline of the electrically-induced [Ca(2+)](i) transient and slowed down the recovery of the electrically-induced [Ca(2+)](i) transient after administration of caffeine. In addition, MI/A prolonged the decline of caffeine induced [Ca(2+)](i) transient, an indication of Na(+)-Ca(2+) exchange activity, and UP prevented it. So UP, that confers cardioprotection, prevented the changes induced by MI/A. With the exception of Ca(2+)-spark, which was not studied, the effects of MI/AP are the same as those of UP. 4. It is concluded that pharmacological preconditioning with U(50), that confers immediate cardioprotection, prevents changes of Ca(2+) homeostasis altered by MI/A in the rat heart. This may be responsible, at least partly, for the cardioprotective action. 5. The study also provided evidence that MI/A causes mobilization of Ca(2+) from SR to cytoplasm causing Ca(2+)-overload which may be due to reduced Ca(2+)-uptake by SR. MI/A also reduces spontaneous and electrically induced Ca(2+) release from SR.
Persistent Identifierhttp://hdl.handle.net/10722/49308
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHo, JCSen_HK
dc.contributor.authorWu, Sen_HK
dc.contributor.authorKam, KWLen_HK
dc.contributor.authorSham, Jen_HK
dc.contributor.authorWong, TMen_HK
dc.date.accessioned2008-06-12T06:39:01Z-
dc.date.available2008-06-12T06:39:01Z-
dc.date.issued2002en_HK
dc.identifier.citationBritish Journal of Pharmacology, 2002, v. 137 n. 6, p. 739-748en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49308-
dc.description.abstract1. The effects of pharmacological preconditioning with U50488H (U(50)), a selective kappa-opioid receptor agonist, on Ca(2+) homeostasis in rat ventricular myocytes subjected for 9 min to metabolic inhibition (MI) and anoxia (A), consequences of ischaemia, were studied and compared with those of preconditioning with brief periods of MI/A. 2. Precondition with 30 micro M of U(50) for three cycles of 1 min each cycle separated by 3 min of recovery (UP) significantly increased the percentage of non-blue cells following MI/A. The effect of UP is the same as that of preconditioning with an inhibitor of glycolysis and an oxygen scavenger for three 1-min cycles separated by three-minute recovery (MI/AP). The results indicate that like MI/AP, UP also confers cardioprotection. 3. MI/A increased intracellular Ca(2+) ([Ca(2+)](i)) and reduced the amplitude of caffeine-induced [Ca(2+)](i) transients, an indication of Ca(2+) content in the sarcoplasmic reticulum (SR). MI/A also reduced the electrically-induced [Ca(2+)](i) transient, that indicates Ca(2+)-release during excitation-contraction coupling, and Ca(2+) sparks in unstimulated myocytes, that indicates spontaneous Ca(2+)-release from SR. It also prolonged the decline of the electrically-induced [Ca(2+)](i) transient and slowed down the recovery of the electrically-induced [Ca(2+)](i) transient after administration of caffeine. In addition, MI/A prolonged the decline of caffeine induced [Ca(2+)](i) transient, an indication of Na(+)-Ca(2+) exchange activity, and UP prevented it. So UP, that confers cardioprotection, prevented the changes induced by MI/A. With the exception of Ca(2+)-spark, which was not studied, the effects of MI/AP are the same as those of UP. 4. It is concluded that pharmacological preconditioning with U(50), that confers immediate cardioprotection, prevents changes of Ca(2+) homeostasis altered by MI/A in the rat heart. This may be responsible, at least partly, for the cardioprotective action. 5. The study also provided evidence that MI/A causes mobilization of Ca(2+) from SR to cytoplasm causing Ca(2+)-overload which may be due to reduced Ca(2+)-uptake by SR. MI/A also reduces spontaneous and electrically induced Ca(2+) release from SR.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.subjectAnoxiaen_HK
dc.subjectMetabolic inhibitionen_HK
dc.subjectCa2+ homeostasisen_HK
dc.subjectVentricular myocyteen_HK
dc.subjectCa2+ sparken_HK
dc.titleEffects of pharmacological preconditioning with U50488H on calcium homeostasis in rat ventricular myocytes subjected to metabolic inhibition and anoxiaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-1188&volume=137&issue=6&spage=739&epage=748&date=2002&atitle=Effects+of+pharmacological+preconditioning+with+U50488H+on+calcium+homeostasis+in+rat+ventricular+myocytes+subjected+to+metabolic+inhibition+and+anoxiaen_HK
dc.identifier.emailWu, S: swua@hkucc.hku.hken_HK
dc.identifier.emailKam, KWL: kam_wan_lung@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.0704945en_HK
dc.identifier.pmid12411403-
dc.identifier.pmcidPMC1573565en_HK
dc.identifier.scopuseid_2-s2.0-0036854465-
dc.identifier.hkuros82591-
dc.identifier.isiWOS:000179326300002-

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