| Exercise-induced expression of cardiac ATP-sensitive potassium channels promotes action potential shortening and energy conservation. | |
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MedLine Citation:
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PMID: 21439969 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Physical activity is one of the most important determinants of cardiac function. The ability of the heart to increase delivery of oxygen and metabolic fuels relies on an array of adaptive responses necessary to match bodily demand while avoiding exhaustion of cardiac resources. The ATP-sensitive potassium (K(ATP)) channel has the unique ability to adjust cardiac membrane excitability in accordance with ATP and ADP levels, and up-regulation of its expression that occurs in response to exercise could represent a critical element of this adaption. However, the mechanism by which K(ATP) channel expression changes result in a beneficial effect on cardiac excitability and function remains to be established. Here, we demonstrate that an exercise-induced rise in K(ATP) channel expression enhanced the rate and magnitude of action potential shortening in response to heart rate acceleration. This adaptation in membrane excitability promoted significant reduction in cardiac energy consumption under escalating workloads. Genetic disruption of normal K(ATP) channel pore function abolished the exercise-related changes in action potential duration adjustment and caused increased cardiac energy consumption. Thus, an expression-driven enhancement in the K(ATP) channel-dependent membrane response to alterations in cardiac workload represents a previously unrecognized mechanism for adaptation to physical activity and a potential target for cardioprotection. |
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Authors:
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Leonid V Zingman; Zhiyong Zhu; Ana Sierra; Elizabeth Stepniak; Colin M-L Burnett; Gennadiy Maksymov; Mark E Anderson; William A Coetzee; Denice M Hodgson-Zingman |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2011-03-23 |
Journal Detail:
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Title: Journal of molecular and cellular cardiology Volume: 51 ISSN: 1095-8584 ISO Abbreviation: J. Mol. Cell. Cardiol. Publication Date: 2011 Jul |
Date Detail:
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Created Date: 2011-05-27 Completed Date: 2011-09-14 Revised Date: 2012-12-11 |
Medline Journal Info:
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Nlm Unique ID: 0262322 Medline TA: J Mol Cell Cardiol Country: England |
Other Details:
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Languages: eng Pagination: 72-81 Citation Subset: IM |
Copyright Information:
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Copyright © 2011 Elsevier Ltd. All rights reserved. |
Affiliation:
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Department of Internal Medicine, University of Iowa, Carver College of Medicine, Iowa City, IA 52242, USA. leonid-zingman@uiowa.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Action Potentials* Animals Energy Metabolism* Heart / physiopathology* KATP Channels / biosynthesis, genetics, metabolism* Membranes / metabolism Mice Mice, Transgenic Myocardium / metabolism Patch-Clamp Techniques Physical Conditioning, Animal* Polymerase Chain Reaction |
| Grant Support | |
ID/Acronym/Agency:
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HL085820/HL/NHLBI NIH HHS; HL092286/HL/NHLBI NIH HHS; HL093368/HL/NHLBI NIH HHS; K08 HL092286-05/HL/NHLBI NIH HHS; K08 HL093368/HL/NHLBI NIH HHS; K08 HL093368-04/HL/NHLBI NIH HHS; L30 HL085940-03/HL/NHLBI NIH HHS; R01 HL070250-10/HL/NHLBI NIH HHS; R01 HL079031-06/HL/NHLBI NIH HHS; R01 HL085820/HL/NHLBI NIH HHS; R01 HL085820-04/HL/NHLBI NIH HHS; R01 HL085820-05/HL/NHLBI NIH HHS; R01 HL096652-04/HL/NHLBI NIH HHS; R01 HL113089/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/KATP Channels |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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