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dc.contributor.authorHarrison, Glennen_US
dc.contributor.authorH. van Wijhe, Michielen_US
dc.contributor.authorGroot, Basen_US
dc.contributor.authorJ. Dijk, Francinaen_US
dc.contributor.authorA. Gustafson, Lorien_US
dc.contributor.authorH. G. M. van Beek, Johannesen_US
dc.contributor.editorD R Harder, David Harder, Brenda B. Rauneren_US
dc.date.accessioned2017-05-03T11:37:00Z
dc.date.available2017-05-03T11:37:00Z
dc.date.issued2003en_US
dc.identifier.issn03636135en_US
dc.identifier.urihttp://hdl.handle.net/10072/6189
dc.description.abstractCreatine kinase (CK) and glycolysis represent important energy-buffering processes in the cardiac myocyte. Although the role of compartmentalized CK in energy transfer has been investigated intensely, similar duties for intracellular glycolysis have not been demonstrated. By measuring the response time of mitochondrial oxygen consumption to dynamic workload jumps (tmito) in isolated rabbit hearts, we studied the effect of inhibiting energetic systems (CK and/or glycolysis) on transcytosolic signal transduction that couples cytosolic ATP hydrolysis to activation of oxidative phosphorylation. Tyrode-perfused hearts were exposed to 15 min of the following: 1) 0.4 mM iodoacetamide (IA; n = 6) to block CK (CK activity <3% vs. control), 2) 0.3 mM iodoacetic acid (IAA; n = 5) to inhibit glycolysis (GAPDH activity <3% vs. control), or 3) vehicle (control, n = 7) at 37î Pretreatment tmito was similar across groups at 4.3 ᠰ.3 s (means ᠓E). No change in tmito was observed in control hearts; however, in IAA- and IA-treated hearts, tmito decreased by 15 ᠳ% and 40 ᠵ%, respectively (P < 0.05 vs. control), indicating quicker energy supply-demand signaling in the absence of ADP/ATP buffering by CK or glycolysis. The faster response times in IAA and IA groups were independent of the size of the workload jump, and the increase in myocardial oxygen consumption during workload steps was unaffected by CK or glycolysis blockade. Contractile function was compromised by IAA and IA treatment versus control, with contractile reserve (defined as increase in rate-pressure product during a standard heart rate jump) reduced to 80 ᠸ% and 80 ᠱ0% of baseline, respectively (P < 0.05 vs. control), and significant elevations in end-diastolic pressure, suggesting raised ADP concentration. These results demonstrate that buffering of phosphate metabolites by glycolysis in the cytosol contributes appreciably to slower mitochondrial activation and may enhance contractile efficiency during increased cardiac workloads. Glycolysis may therefore play a role similar to CK in heart muscle.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_US
dc.languageEnglishen_US
dc.language.isoen_US
dc.publisherAmerican Physiological Societyen_US
dc.publisher.placeUntied Statesen_US
dc.publisher.urihttp://ajpheart.physiology.org/content/285/2/H883en_US
dc.relation.ispartofpagefrom883en_US
dc.relation.ispartofpageto890en_US
dc.relation.ispartofjournalAmerican Journal of Physiology: Heart and Circulatory Physiologyen_US
dc.relation.ispartofvolume285en_US
dc.subject.fieldofresearchcode321003en_US
dc.titleGlycolytic buffering affects cardiac bioenergetics signaling and contractile reserve similar to creatine kinaseen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.rights.copyrightSelf-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author[s] for more information.en_US
gro.date.issued2015-02-05T03:42:24Z
gro.hasfulltextNo Full Text


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