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Oxidative injury due to chronic nitric oxide synthase inhibition in rat: effect of regular exercise on the heart.
Biochim Biophys Acta. 2002 May 21; 1587(1):75-82.BB

Abstract

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.

Authors+Show Affiliations

Department of Surgery, School of Medicine, Southern Illinois University, 800 North Rutledge St., Springfield, IL 62794-9638, USA. khusain@siumed.eduNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12009427

Citation

Husain, Kazim, and Stephen R. Hazelrigg. "Oxidative Injury Due to Chronic Nitric Oxide Synthase Inhibition in Rat: Effect of Regular Exercise On the Heart." Biochimica Et Biophysica Acta, vol. 1587, no. 1, 2002, pp. 75-82.
Husain K, Hazelrigg SR. Oxidative injury due to chronic nitric oxide synthase inhibition in rat: effect of regular exercise on the heart. Biochim Biophys Acta. 2002;1587(1):75-82.
Husain, K., & Hazelrigg, S. R. (2002). Oxidative injury due to chronic nitric oxide synthase inhibition in rat: effect of regular exercise on the heart. Biochimica Et Biophysica Acta, 1587(1), 75-82.
Husain K, Hazelrigg SR. Oxidative Injury Due to Chronic Nitric Oxide Synthase Inhibition in Rat: Effect of Regular Exercise On the Heart. Biochim Biophys Acta. 2002 May 21;1587(1):75-82. PubMed PMID: 12009427.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxidative injury due to chronic nitric oxide synthase inhibition in rat: effect of regular exercise on the heart. AU - Husain,Kazim, AU - Hazelrigg,Stephen R, PY - 2002/5/16/pubmed PY - 2002/8/7/medline PY - 2002/5/16/entrez SP - 75 EP - 82 JF - Biochimica et biophysica acta JO - Biochim Biophys Acta VL - 1587 IS - 1 N2 - 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. SN - 0006-3002 UR - https://www.unboundmedicine.com/medline/citation/12009427/Oxidative_injury_due_to_chronic_nitric_oxide_synthase_inhibition_in_rat:_effect_of_regular_exercise_on_the_heart_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0925443902000704 DB - PRIME DP - Unbound Medicine ER -