Document Detail

Exercise protects against myocardial ischemia-reperfusion injury via stimulation of β(3)-adrenergic receptors and increased nitric oxide signaling: role of nitrite and nitrosothiols.
MedLine Citation:
PMID:  21527738     Owner:  NLM     Status:  MEDLINE    
RATIONALE: Exercise training confers sustainable protection against ischemia-reperfusion injury in animal models and has been associated with improved survival following a heart attack in humans. It is still unclear how exercise protects the heart, but it is apparent that endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) play a role.
OBJECTIVE: To determine the role of β(3)-adrenergic receptors (β(3)-ARs), eNOS activation, and NO metabolites (nitrite and nitrosothiols) in the sustained cardioprotective effects of exercise.
METHODS AND RESULTS: Here we show that voluntary exercise reduces myocardial injury in mice following a 4-week training period and that these protective effects can be sustained for at least 1 week following the cessation of the training. The sustained cardioprotective effects of exercise are mediated by alterations in the phosphorylation status of eNOS (increase in serine 1177 and decrease in threonine 495), leading to an increase in NO generation and storage of NO metabolites (nitrite and nitrosothiols) in the heart. Further evidence revealed that the alterations in eNOS phosphorylation status and NO generation were mediated by β(3)-AR stimulation and that in response to exercise a deficiency of β(3)-ARs leads to an exacerbation of myocardial infarction following ischemia-reperfusion injury.
CONCLUSIONS: Our findings clearly demonstrate that exercise protects the heart against myocardial ischemia-reperfusion injury by stimulation of β(3)-ARs and increased cardiac storage of nitric oxide metabolites (ie, nitrite and nitrosothiols).
John W Calvert; Marah E Condit; Juan Pablo Aragón; Chad K Nicholson; Bridgette F Moody; Rebecca L Hood; Amy L Sindler; Susheel Gundewar; Douglas R Seals; Lili A Barouch; David J Lefer
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-04-28
Journal Detail:
Title:  Circulation research     Volume:  108     ISSN:  1524-4571     ISO Abbreviation:  Circ. Res.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-06-10     Completed Date:  2011-08-12     Revised Date:  2014-09-19    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1448-58     Citation Subset:  IM    
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MeSH Terms
Enzyme Activation
Mice, Knockout
Myocardial Reperfusion Injury / genetics,  metabolism,  prevention & control*
Nitric Oxide / genetics,  metabolism*
Nitric Oxide Synthase Type III / genetics,  metabolism
Nitrites / metabolism*
Nitroso Compounds / metabolism*
Physical Conditioning, Animal*
Receptors, Adrenergic, beta-3 / genetics,  metabolism*
Time Factors
Grant Support
1R01HL093579-01/HL/NHLBI NIH HHS; 1R01HL098481-01/HL/NHLBI NIH HHS; 5R01HL-092141-02/HL/NHLBI NIH HHS; R01 HL060849/HL/NHLBI NIH HHS; R01 HL060849-09/HL/NHLBI NIH HHS; R01 HL092141/HL/NHLBI NIH HHS; R01 HL092141-02/HL/NHLBI NIH HHS; R01 HL093579/HL/NHLBI NIH HHS; R01 HL093579-02/HL/NHLBI NIH HHS; R01 HL098481/HL/NHLBI NIH HHS; R01 HL098481-02/HL/NHLBI NIH HHS
Reg. No./Substance:
0/Nitrites; 0/Nitroso Compounds; 0/Receptors, Adrenergic, beta-3; 31C4KY9ESH/Nitric Oxide; EC protein, human; EC Oxide Synthase Type III; EC protein, mouse
Comment In:
Circ Res. 2011 Jun 10;108(12):1414-6   [PMID:  21659650 ]

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