Glycolytic buffering affects cardiac bioenergetics signaling and contractile reserve similar to creatine kinase

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Title Glycolytic buffering affects cardiac bioenergetics signaling and contractile reserve similar to creatine kinase
Author Harrison, Glenn; Wijhe, Michiel H. van; Groot, Bas de; Dijk, Francina J.; Gustafson, Lori A.; Beek, Johannes H. G. M. van
Journal Name American Journal of Physiology: Heart and Circulatory Physiology
Editor D R Harder, David Harder, Brenda B. Rauner
Year Published 2003
Place of publication Untied States
Publisher American Physiological Society
Abstract Creatine 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 37°C. Pretreatment tmito was similar across groups at 4.3 ± 0.3 s (means ± SE). No change in tmito was observed in control hearts; however, in IAA- and IA-treated hearts, tmito decreased by 15 ± 3% and 40 ± 5%, 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 ± 8% and 80 ± 10% 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.
Peer Reviewed Yes
Published Yes
Publisher URI
Copyright Statement Self-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.
Volume 285
Page from 883
Page to 890
ISSN 0363-6135
Date Accessioned 2004-03-19
Date Available 2015-02-05T03:42:24Z
Language en_US
Research Centre Menzies Health Institute Qld
Faculty Griffith Health Faculty
Subject PRE2009-Cardiology (incl. Cardiovascular Diseases)
Publication Type Journal Articles (Refereed Article)
Publication Type Code c1

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