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Article: Chronic intermittent hypoxia alters Ca2+ handling in rat cardiomyocytes by augmented Na+/Ca2+ exchange and ryanodine receptor activities in ischemia-reperfusion

TitleChronic intermittent hypoxia alters Ca2+ handling in rat cardiomyocytes by augmented Na+/Ca2+ exchange and ryanodine receptor activities in ischemia-reperfusion
Authors
KeywordsCardioprotection
Intracellular calcium
Issue Date2007
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/
Citation
American Journal Of Physiology - Cell Physiology, 2007, v. 292 n. 6, p. C2046-C2056 How to Cite?
AbstractThis study examined Ca2+ handling mechanisms involved in cardioprotection induced by chronic intermittent hypoxia (CIH) against ischemia-reperfusion (I/R) injury. Adult male Sprague-Dawley rats were exposed to 10% inspired O2 continuously for 6 h daily from 3, 7, and 14 days. In isolated perfused hearts subjected to I/R, CIH-induced cardioprotection was most significant in the 7-day group with less infarct size and lactate dehydrogenase release, compared with the normoxic group. The I/R-induced alterations in diastolic Ca2+ level, amplitude, time-to-peak, and the decay time of both electrically and caffeine-induced Ca2+ transients measured by spectrofluorometry in isolated ventricular myocytes of the 7-day CIH group were less than that of the normoxic group, suggesting an involvement of altered Ca2+ handling of the sarcoplasmic reticulum (SR) and sarcolemma. We further determined the protein expression and activity of 45Ca2+ flux of SR-Ca2+-ATPase, ryanodine receptor (RyR) and sarcolemmal Na+/Ca2+ exchange (NCX) in ventricular myocytes from the CIH and normoxic groups before and during I/R. There were no changes in expression levels of the Ca2+-handling proteins but significant increases in the RyR and NCX activities were remarkable during I/R in the CIH but not the normoxic group. The augmented RyR and NCX activities were abolished, respectively, by PKA inhibitor (0.5 μM KT5720 or 0.5 μM PKI14-22) and PKC inhibitor (5 μM chelerythrine chloride or 0.2 μM calphostin C) but not by Ca2+/calmodulin-dependent protein kinase II inhibitor KN-93 (1 μM). Thus, CIH confers cardioprotection against I/R injury in rat cardiomyocytes by altered Ca2+ handling with augmented RyR and NCX activities via protein kinase activation. Copyright © 2007 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/81163
ISSN
2015 Impact Factor: 3.395
2015 SCImago Journal Rankings: 1.893
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYeung, HMen_HK
dc.contributor.authorKravtsov, GMen_HK
dc.contributor.authorNg, KMen_HK
dc.contributor.authorWong, TMen_HK
dc.contributor.authorFung, MLen_HK
dc.date.accessioned2010-09-06T08:14:33Z-
dc.date.available2010-09-06T08:14:33Z-
dc.date.issued2007en_HK
dc.identifier.citationAmerican Journal Of Physiology - Cell Physiology, 2007, v. 292 n. 6, p. C2046-C2056en_HK
dc.identifier.issn0363-6143en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81163-
dc.description.abstractThis study examined Ca2+ handling mechanisms involved in cardioprotection induced by chronic intermittent hypoxia (CIH) against ischemia-reperfusion (I/R) injury. Adult male Sprague-Dawley rats were exposed to 10% inspired O2 continuously for 6 h daily from 3, 7, and 14 days. In isolated perfused hearts subjected to I/R, CIH-induced cardioprotection was most significant in the 7-day group with less infarct size and lactate dehydrogenase release, compared with the normoxic group. The I/R-induced alterations in diastolic Ca2+ level, amplitude, time-to-peak, and the decay time of both electrically and caffeine-induced Ca2+ transients measured by spectrofluorometry in isolated ventricular myocytes of the 7-day CIH group were less than that of the normoxic group, suggesting an involvement of altered Ca2+ handling of the sarcoplasmic reticulum (SR) and sarcolemma. We further determined the protein expression and activity of 45Ca2+ flux of SR-Ca2+-ATPase, ryanodine receptor (RyR) and sarcolemmal Na+/Ca2+ exchange (NCX) in ventricular myocytes from the CIH and normoxic groups before and during I/R. There were no changes in expression levels of the Ca2+-handling proteins but significant increases in the RyR and NCX activities were remarkable during I/R in the CIH but not the normoxic group. The augmented RyR and NCX activities were abolished, respectively, by PKA inhibitor (0.5 μM KT5720 or 0.5 μM PKI14-22) and PKC inhibitor (5 μM chelerythrine chloride or 0.2 μM calphostin C) but not by Ca2+/calmodulin-dependent protein kinase II inhibitor KN-93 (1 μM). Thus, CIH confers cardioprotection against I/R injury in rat cardiomyocytes by altered Ca2+ handling with augmented RyR and NCX activities via protein kinase activation. Copyright © 2007 the American Physiological Society.en_HK
dc.languageengen_HK
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/en_HK
dc.relation.ispartofAmerican Journal of Physiology - Cell Physiologyen_HK
dc.subjectCardioprotectionen_HK
dc.subjectIntracellular calciumen_HK
dc.titleChronic intermittent hypoxia alters Ca2+ handling in rat cardiomyocytes by augmented Na+/Ca2+ exchange and ryanodine receptor activities in ischemia-reperfusionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0363-6143&volume=292&spage=C2046&epage=2056&date=2007&atitle=Chronic+intermittent+hypoxia+alters+Ca2++handling+in+rat+cardiomyocytes+by+augmented+Na+/Ca2++exchange+and+ryanodine+receptor+activity+in+ischemia-reperfusionen_HK
dc.identifier.emailNg, KM: skykmng@hkucc.hku.hken_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityNg, KM=rp01670en_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1152/ajpcell.00458.2006en_HK
dc.identifier.pmid17267548-
dc.identifier.scopuseid_2-s2.0-34447517769en_HK
dc.identifier.hkuros128686en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34447517769&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume292en_HK
dc.identifier.issue6en_HK
dc.identifier.spageC2046en_HK
dc.identifier.epageC2056en_HK
dc.identifier.isiWOS:000247936600006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYeung, HM=7102212148en_HK
dc.identifier.scopusauthoridKravtsov, GM=7003811092en_HK
dc.identifier.scopusauthoridNg, KM=25122990200en_HK
dc.identifier.scopusauthoridWong, TM=7403531434en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK

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