Document Detail

Oxidative injury due to chronic nitric oxide synthase inhibition in rat: effect of regular exercise on the heart.
MedLine Citation:
PMID:  12009427     Owner:  NLM     Status:  MEDLINE    
Many individuals with cardiac diseases undergo periodic physical conditioning with or without medication. Therefore, this study investigated the interaction of physical training and chronic nitric oxide synthase (NOS) inhibitor (nitro-L-arginine methyl ester, L-NAME) treatment on blood pressure (BP), heart rate (HR) and cardiac oxidant/antioxidant systems in rats. Fisher 344 rats were divided into four groups and treated as follows: (1) sedentary control (SC), (2) exercise training (ET) for 8 weeks, (3) L-NAME (10 mg/kg, s.c. for 8 weeks) and (4) ET+L-NAME. BP and HR were monitored with tail-cuff method. The animals were sacrificed 24 h after last treatments and hearts were isolated and analyzed. Physical conditioning significantly increased respiratory exchange ratio (RER), cardiac nitric oxide (NO) levels, NOS activity and endothelial (eNOS) and inducible (iNOS) protein expression. Training significantly enhanced cardiac glutathione (GSH) levels, GSH/GSSG ratio and up-regulation of cardiac copper/zinc-superoxide dismutase (CuZn-SOD), manganese (Mn)-SOD, catalase (CAT), glutathione peroxidase (GSH-Px) activity and protein expression. Training also caused depletion of cardiac malondialdehyde (MDA) and protein carbonyls. Chronic L-NAME administration resulted in depletion of cardiac NO level, NOS activity, eNOS, nNOS and iNOS protein expression, GSH/GSSG ratio and down-regulation of cardiac CuZn-SOD, Mn-SOD, CAT, GSH-PX, glutathione-S-transferase (GST) activity and protein expression. Chronic L-NAME administration enhanced cardiac xanthine oxidase (XO) activity, MDA levels and protein carbonyls. These biochemical changes were accompanied by increases in BP and HR after L-NAME administration. Interaction of training and NOS inhibitor treatment resulted in normalization of BP, HR and up-regulation of cardiac antioxidant defense system. The data suggest that physical conditioning attenuated the oxidative injury caused by chronic NOS inhibition by up-regulating the cardiac antioxidant defense system and lowering the BP and HR in rats.
Kazim Husain; Stephen R Hazelrigg
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Biochimica et biophysica acta     Volume:  1587     ISSN:  0006-3002     ISO Abbreviation:  Biochim. Biophys. Acta     Publication Date:  2002 May 
Date Detail:
Created Date:  2002-05-15     Completed Date:  2002-08-06     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0217513     Medline TA:  Biochim Biophys Acta     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  75-82     Citation Subset:  IM    
Department of Surgery, School of Medicine, Southern Illinois University, 800 North Rutledge St., Springfield, IL 62794-9638, USA.
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MeSH Terms
Blood Pressure / drug effects
Catalase / metabolism
Glutathione / metabolism
Heart / physiology*
Heart Rate / drug effects
Malondialdehyde / analysis
NG-Nitroarginine Methyl Ester / pharmacology*
Nitric Oxide / metabolism
Nitric Oxide Synthase / antagonists & inhibitors*,  biosynthesis
Oxidative Stress*
Physical Conditioning, Animal*
Rats, Inbred F344
Superoxide Dismutase / metabolism
Reg. No./Substance:
10102-43-9/Nitric Oxide; 50903-99-6/NG-Nitroarginine Methyl Ester; 542-78-9/Malondialdehyde; 70-18-8/Glutathione; EC; EC Oxide Synthase; EC Dismutase

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