Document Detail

Angiotensin preconditioning of the heart: evidence for redox signaling.
MedLine Citation:
PMID:  16456238     Owner:  NLM     Status:  MEDLINE    
Angiotensin II (Ang II) has been found to exert preconditioning-like effect on mammalian hearts. Diverse mechanisms are known to exist to explain the cardioprotective abilities of Ang II preconditioning. The present study hypothesized, based on the recent report that Ang II generates reactive oxygen species (ROS) through NADPH oxidase, that Ang II preconditioning occurs through redox cycling. To test this hypothesis, a group of rat hearts was treated with Ang II in the absence or presence of an NADPH oxidase inhibitor, apocynin; or a cell-permeable ROS scavenger, N-acetyl cysteine (NAC). Ang II pretreatment improved postischemic ventricular recovery; reduced myocardial infarction; and decreased the number of cardiomyocyte apoptosis, indicating its ability to precondition the heart against ischemic injury. Both apocynin and NAC almost abolished the preconditioning ability of Ang II. Ang II resulted in increase in ROS activity in the heart, which was reduced by either NAC or apocynin. Ang II also increased both the NADPH oxidase subunits gp91 phox and p22phox mRNA expression, which was abolished with apocynin and NAC. Our results thus demonstrate that the Ang II preconditioning was associated with enhanced ROS activities and increased NADPH oxidase subunits p22phox and gp91phox expression. Both NAC and apocynin reduced ROS activities simultaneously abolishing preconditioning ability of Ang II, suggesting that Ang II preconditioning occurs through redox cycling. That both NAC and apocynin reduced ROS activities and abolished Ang II-mediated increase in p22phox and gp91phox activity further suggest that such redox cycling occurs via both NADPH oxidase-dependent and -independent pathways.
Samarjit Das; Richard M Engelman; Nilanjana Maulik; Dipak K Das
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Cell biochemistry and biophysics     Volume:  44     ISSN:  1085-9195     ISO Abbreviation:  Cell Biochem. Biophys.     Publication Date:  2006  
Date Detail:
Created Date:  2006-02-03     Completed Date:  2006-04-05     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9701934     Medline TA:  Cell Biochem Biophys     Country:  United States    
Other Details:
Languages:  eng     Pagination:  103-10     Citation Subset:  IM    
Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, CT, USA.
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MeSH Terms
Acetophenones / pharmacology
Acetylcysteine / pharmacology
Angiotensin II / pharmacology*
Antioxidants / pharmacology
Apoptosis / drug effects
Gene Expression / drug effects
Heart / drug effects
Heart Rate / drug effects
Ischemic Preconditioning, Myocardial*
Membrane Glycoproteins / genetics
Membrane Transport Proteins / genetics
Myocardial Infarction / etiology,  metabolism,  pathology
Myocardial Reperfusion Injury / complications
Myocardium / metabolism
Myocytes, Cardiac / drug effects,  metabolism
NADPH Oxidase / genetics
Phosphoproteins / genetics
RNA, Messenger / genetics,  metabolism
Rats, Sprague-Dawley
Reactive Oxygen Species / metabolism
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction / drug effects*,  physiology
Ventricular Function, Left / drug effects
Ventricular Remodeling / drug effects
Grant Support
Reg. No./Substance:
0/Acetophenones; 0/Antioxidants; 0/Membrane Glycoproteins; 0/Membrane Transport Proteins; 0/Phosphoproteins; 0/RNA, Messenger; 0/Reactive Oxygen Species; 11128-99-7/Angiotensin II; 498-02-2/acetovanillone; 616-91-1/Acetylcysteine; EC 1.6.-/Cybb protein, rat; EC protein, human; EC Oxidase

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