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Article: Calcium homeostasis in rat cardiomyocytes during chronic hypoxia: A time course study

TitleCalcium homeostasis in rat cardiomyocytes during chronic hypoxia: A time course study
Authors
Issue Date2003
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/
Citation
American Journal Of Physiology - Cell Physiology, 2003, v. 285 n. 6 54-6, p. C1420-C1428 How to Cite?
AbstractThe present study determined Ca2+ handling in the hearts of rats subjected to chronic hypoxia (CH). Spectrofluorometry was used to measure intracellular Ca2+ concentration ([Ca2+]i) and its responses to electrical stimulation, caffeine, and isoproterenol in myocytes from the right ventricle of rats breathing 10% oxygen for 1, 3, 7, 14, 21, 28, and 56 days and age-matched controls. The protein expression of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) and its ryanodine receptor (RyR) were measured. The uptake of 45Ca2+ by SERCA, release by RyR, and extrusion by Na+/Ca2+ exchange (NCX) were determined. It was found that Ca2+ homeostasis and Ca 2+ responses to β-adrenoceptor stimulation reached a new equilibrium after 4 wk of CH. Ca2+ content in the sarcoplasmic reticulum (SR) was reduced, but cytosolic Ca2+ remained unchanged after CH. Expression of SERCA and its Ca2+ uptake, Ca2+ release via RyR, and NCX activity were suppressed by CH. The results indicate impaired Ca2+ handling, which may be responsible for the attenuated Ca2+ responses to β-adrenoceptor stimulation in CH.
Persistent Identifierhttp://hdl.handle.net/10722/171718
ISSN
2015 Impact Factor: 3.395
2015 SCImago Journal Rankings: 1.893
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPei, JMen_US
dc.contributor.authorKravtsov, GMen_US
dc.contributor.authorWu, Sen_US
dc.contributor.authorDas, Ren_US
dc.contributor.authorFung, MLen_US
dc.contributor.authorWong, TMen_US
dc.date.accessioned2012-10-30T06:16:35Z-
dc.date.available2012-10-30T06:16:35Z-
dc.date.issued2003en_US
dc.identifier.citationAmerican Journal Of Physiology - Cell Physiology, 2003, v. 285 n. 6 54-6, p. C1420-C1428en_US
dc.identifier.issn0363-6143en_US
dc.identifier.urihttp://hdl.handle.net/10722/171718-
dc.description.abstractThe present study determined Ca2+ handling in the hearts of rats subjected to chronic hypoxia (CH). Spectrofluorometry was used to measure intracellular Ca2+ concentration ([Ca2+]i) and its responses to electrical stimulation, caffeine, and isoproterenol in myocytes from the right ventricle of rats breathing 10% oxygen for 1, 3, 7, 14, 21, 28, and 56 days and age-matched controls. The protein expression of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) and its ryanodine receptor (RyR) were measured. The uptake of 45Ca2+ by SERCA, release by RyR, and extrusion by Na+/Ca2+ exchange (NCX) were determined. It was found that Ca2+ homeostasis and Ca 2+ responses to β-adrenoceptor stimulation reached a new equilibrium after 4 wk of CH. Ca2+ content in the sarcoplasmic reticulum (SR) was reduced, but cytosolic Ca2+ remained unchanged after CH. Expression of SERCA and its Ca2+ uptake, Ca2+ release via RyR, and NCX activity were suppressed by CH. The results indicate impaired Ca2+ handling, which may be responsible for the attenuated Ca2+ responses to β-adrenoceptor stimulation in CH.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Cell Physiologyen_US
dc.subject.meshAdrenergic Beta-Agonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Metabolismen_US
dc.subject.meshCaffeine - Pharmacologyen_US
dc.subject.meshCalcium - Analysis - Metabolismen_US
dc.subject.meshCalcium-Transporting Atpases - Biosynthesis - Drug Effectsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCentral Nervous System Stimulants - Pharmacologyen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshHomeostasis - Physiologyen_US
dc.subject.meshIntracellular Fluid - Chemistry - Drug Effectsen_US
dc.subject.meshIsoproterenol - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMyocytes, Cardiac - Drug Effects - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshRyanodine Receptor Calcium Release Channel - Biosynthesis - Drug Effectsen_US
dc.subject.meshSarcoplasmic Reticulum - Metabolismen_US
dc.subject.meshSarcoplasmic Reticulum Calcium-Transporting Atpasesen_US
dc.subject.meshSodium-Calcium Exchanger - Metabolismen_US
dc.subject.meshSpectrometry, Fluorescenceen_US
dc.subject.meshTime Factorsen_US
dc.titleCalcium homeostasis in rat cardiomyocytes during chronic hypoxia: A time course studyen_US
dc.typeArticleen_US
dc.identifier.emailFung, ML:fungml@hkucc.hku.hken_US
dc.identifier.emailKravtsov, GM: gmkravts@HKUCC.hku.hk-
dc.identifier.emailDas, R: raptidas@hkucc.hku.hk-
dc.identifier.emailWong, TM: tm.wong@hkuspace.hku.hk-
dc.identifier.authorityFung, ML=rp00433en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1152/ajpcell.00534.2002-
dc.identifier.pmid14600077-
dc.identifier.scopuseid_2-s2.0-0242426654en_US
dc.identifier.hkuros88098-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0242426654&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume285en_US
dc.identifier.issue6 54-6en_US
dc.identifier.spageC1420en_US
dc.identifier.epageC1428en_US
dc.identifier.isiWOS:000186343600008-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridPei, JM=7103299061en_US
dc.identifier.scopusauthoridKravtsov, GM=7003811092en_US
dc.identifier.scopusauthoridWu, S=7408443898en_US
dc.identifier.scopusauthoridDas, R=7202061890en_US
dc.identifier.scopusauthoridFung, ML=7101955092en_US
dc.identifier.scopusauthoridWong, TM=7403531434en_US

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