Document Detail


Hydrogen peroxide generated from cardiac myocytes impacts metabolic dilation in coronary arterioles.
MedLine Citation:
PMID:  20379047     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
During oxidative cardiac metabolism, the myocardium produces reactive oxygen species, such as superoxide and hydrogen peroxide (H(2)O(2)). We hypothesized H(2)O(2) is a coronary metabolic dilator linking regulation of coronary tone with myocardium metabolism. Dilation of isolated, pressurized coronary arterioles (76 +/- 10 microm, diameter) in reaction to supernatant collected from enzymatically isolated cardiac myocytes was measured. Isolated rat myocytes were stimulated electrically [unpaced or stimulated at 200, 400 beats/min (bpm)]. H(2)O(2) was significantly generated by pacing (400 bpm n = 11, 9.3 +/- 0.4 microM P < 0.01, versus unpaced) and the addition of this supernatant caused vasodilation (500 microL to 2 mL bath, 14.6 +/- 0.7%, P < 0.01 versus unpaced). Supernatant from unpaced myocytes was not vasoactive. To clarify the source of H(2)O(2), myocytes were also stimulated at 400 bpm following treatment with Mn-TBAP (25 microM), which mimics the action of Mn-SOD, and apocynin (3 mM), an NADPH oxidase inhibitor (n = 11, each). Mn-TBAP increased H(2)O(2) generation in myocyte supernatant stimulated at 400 bpm (12.2 +/- 0.8 microM, P < 0.01 versus 400 bpm stimulation only). Treatment of the myocytes with Mn-TBAP augmented vasodilation by the stimulated myocyte supernatant (19.6 +/- 1.1%, P < 0.01 versus untreated myocyte supernatant). Apocynin did not alter vasodilation to myocyte supernatant. These results suggest that the main source of superoxide by metabolic stimuli is cardiac myocytes and Mn-SOD is a scavenger from superoxide to H(2)O(2). We conclude that H(2)O(2) is a key metabolic vasodilator produced by myocardium.
Authors:
Atsushi Otake; Shu-ichi Saitoh; Yasuchika Takeishi
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  International heart journal     Volume:  51     ISSN:  1349-2365     ISO Abbreviation:  Int Heart J     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-04-09     Completed Date:  2010-05-18     Revised Date:  2010-07-01    
Medline Journal Info:
Nlm Unique ID:  101244240     Medline TA:  Int Heart J     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  125-8     Citation Subset:  IM    
Affiliation:
Department of Cardiology and Hematology, Fukushima Medical University, Fukushima, Fukushima, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arterioles / drug effects*
Cell Culture Techniques
Coronary Circulation / drug effects
Hydrogen Peroxide / pharmacology*
Male
Microcirculation / drug effects
Myocytes, Cardiac / metabolism*
Oxidants / pharmacology*
Oxidative Stress / physiology*
Rats
Rats, Sprague-Dawley
Rats, Wistar
Vasodilation / drug effects*
Chemical
Reg. No./Substance:
0/Oxidants; 7722-84-1/Hydrogen Peroxide

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