Document Detail


Exercise-induced expression of cardiac ATP-sensitive potassium channels promotes action potential shortening and energy conservation.
MedLine Citation:
PMID:  21439969     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
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:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-03-23
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  51     ISSN:  1095-8584     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-05-27     Completed Date:  2011-09-14     Revised Date:  2014-09-13    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  72-81     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Ltd. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
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:
HL085820/HL/NHLBI NIH HHS; HL092286/HL/NHLBI NIH HHS; HL093368/HL/NHLBI NIH HHS; K08 HL092286/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/HL/NHLBI NIH HHS; L30 HL085940-03/HL/NHLBI NIH HHS; R01 HL070250/HL/NHLBI NIH HHS; R01 HL070250-10/HL/NHLBI NIH HHS; R01 HL079031/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/HL/NHLBI NIH HHS; R01 HL096652-04/HL/NHLBI NIH HHS; R01 HL113089/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/KATP Channels
Comments/Corrections

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