Document Detail


Mitochondrial KATP channel inhibition blunts arrhythmia protection in ischemic exercised hearts.
MedLine Citation:
PMID:  20435852     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The mechanisms responsible for anti-arrhythmic protection during ischemia-reperfusion (IR) in exercised hearts are not fully understood. The purpose of this investigation was to examine whether the ATP-sensitive potassium channels in the mitochondria (mito K(ATP)) and sarcolemma (sarc K(ATP)) provide anti-arrhythmic protection in exercised hearts during IR. Male Sprague-Dawley rats were randomly assigned to cardioprotective treadmill exercise or sedentary conditions before IR (I = 20 min, R = 30 min) in vivo. Subsets of exercised animals received pharmacological inhibitors for mito K(ATP) (5-hydroxydecanoate) or sarc K(ATP) (HMR1098) before IR. Blinded analysis of digital ECG tracings revealed that mito K(ATP) inhibition blunted the anti-arrhythmic effects of exercise, while sarc K(ATP) inhibition did not. Endogenous antioxidant enzyme activities for total, CuZn, and Mn superoxide dismutase, catalase, and glutathione peroxidase from ischemic and perfused ventricular tissue were not mitigated by IR, although oxidative stress was elevated in sedentary and mito K(ATP)-inhibited hearts from exercised animals. These findings suggest that the mito K(ATP) channel provides anti-arrhythmic protection as part of exercise-mediated cardioprotection against IR. Furthermore, these data suggest that the observed anti-arrhythmic protection may be associated with preservation of redox balance in exercised hearts.
Authors:
John C Quindry; Lindsey Schreiber; Peter Hosick; Jenna Wrieden; J Megan Irwin; Emily Hoyt
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-04-30
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  299     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-06-17     Completed Date:  2010-07-06     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H175-83     Citation Subset:  IM    
Affiliation:
Cardioprotection Laboratory, Department of Kinesiology, Auburn University, Auburn, AL 36849, USA. jcq0001@auburn.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Arrhythmias, Cardiac / etiology,  metabolism,  physiopathology,  prevention & control*
Benzamides / pharmacology
Catalase / metabolism
Decanoic Acids / pharmacology*
Disease Models, Animal
Electrocardiography
Glutathione Peroxidase / metabolism
Hydroxy Acids / pharmacology*
KATP Channels / antagonists & inhibitors,  metabolism
Male
Mitochondria, Heart / drug effects*,  metabolism
Myocardial Reperfusion Injury / complications*,  metabolism,  physiopathology
Myocardium / metabolism*
Oxidation-Reduction
Oxidative Stress / drug effects
Physical Exertion*
Potassium Channel Blockers / pharmacology*
Potassium Channels / drug effects*,  metabolism
Rats
Rats, Sprague-Dawley
Sarcolemma / drug effects,  metabolism
Superoxide Dismutase / metabolism
Grant Support
ID/Acronym/Agency:
HL087256/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Benzamides; 0/Decanoic Acids; 0/HMR 1098; 0/Hydroxy Acids; 0/KATP Channels; 0/Potassium Channel Blockers; 0/Potassium Channels; 0/mitochondrial K(ATP) channel; 624-00-0/5-hydroxydecanoic acid; EC 1.11.1.6/Catalase; EC 1.11.1.9/Glutathione Peroxidase; EC 1.15.1.1/Superoxide Dismutase
Comments/Corrections

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