β-Adrenergic receptors desensitization is not involved in exercise-induced cardiac fatigue: NADPH oxidase-induced oxidative stress as a new trigger
| Autor: | Phillippe Obert, Julien Boissiere, Stéphane Nottin, Anne Sophie Polge, Sandrine Gayrard, Gregory Doucende, Cyril Reboul, Aurélie Goux, Patrice Faure, Stéphane Tanguy, Damien Vitiello |
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| Přispěvatelé: | Laboratoire de bioénergétique fondamentale et appliquée (LBFA), Université Joseph Fourier - Grenoble 1 (UJF)-Institut National de la Santé et de la Recherche Médicale (INSERM), Physiopathologie des adaptations cardiovasculaires à l'Exercice, Avignon Université (AU), Service de Biochimie, Centre Hospitalier Universitaire de Nîmes (CHU Nîmes), Hypoxie et physiopathologies cardiovasculaire et respiratoire, Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Joseph Fourier - Grenoble 1 (UJF) |
| Rok vydání: | 2011 |
| Předmět: |
Male
Physiology myocardial dysfunction β-adrenergic pathway MESH: Physical Conditioning Animal 030204 cardiovascular system & hematology medicine.disease_cause MESH: Isoproterenol MESH: Lipid Peroxidation Lipid peroxidation Ventricular Dysfunction Left chemistry.chemical_compound 0302 clinical medicine Desensitization (telecommunications) MESH: Ventricular Dysfunction Left polycyclic compounds MESH: Animals MESH: NADPH Oxidase MESH: Oxidative Stress NADPH oxidase biology Biochemistry cardiovascular system Cardiac function curve MESH: Troponin I medicine.medical_specialty MESH: Myocardium MESH: Rats Heart Ventricles MESH: Receptors Adrenergic beta Contractility 03 medical and health sciences [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system Physical Conditioning Animal Physiology (medical) Internal medicine Receptors Adrenergic beta medicine Animals Rats Wistar Heart Failure Myocardium Troponin I Isoproterenol Acetophenones NADPH Oxidases MESH: Rats Wistar biochemical phenomena metabolism and nutrition MESH: Male Rats Oxidative Stress Endocrinology chemistry MESH: Acetophenones MESH: Heart Failure Apocynin biology.protein Lipid Peroxidation MESH: Heart Ventricles 030217 neurology & neurosurgery Ex vivo Oxidative stress |
| Zdroj: | Journal of Applied Physiology Journal of Applied Physiology, American Physiological Society, 2011, 111 (5), pp.1242-8. ⟨10.1152/japplphysiol.00449.2011⟩ |
| ISSN: | 1522-1601 8750-7587 |
| DOI: | 10.1152/japplphysiol.00449.2011 |
| Popis: | International audience; Prolonged strenuous exercise (PSE) induces transient left ventricular (LV) dysfunction. Previous studies suggest that β-adrenergic pathway desensitization could be involved in this phenomenon, but it remains to be confirmed. Moreover, other underlying mechanisms involving oxidative stress have been recently proposed. The present study aimed to evaluate the involvement of both the β-adrenergic pathway and NADPH oxidase (Nox) enzyme-induced oxidative stress in myocardial dysfunction in rats following PSE. Rats were divided into 4 groups: controls (Ctrl), 4-h exercised on treadmill (PSE), and 2 groups in which Nox enzyme was inhibited with apocynin treatment (Ctrl APO and PSE APO, respectively). We evaluated cardiac function in vivo and ex vivo during basal conditions and isoproterenol stress. GSH/GSSG ratio, cardiac troponin I (cTnI) release, and lipid peroxidation (MDA) were evaluated. PSE induced a decrease in LV developed pressure, intrinsic myocardial contractility, and relaxation associated with an increase in plasma cTnI release. Our in vivo and ex vivo results demonstrated no differences in myocardial response to isoproterenol and of effective dose 50 between control and PSE rats. Interestingly, the LV dysfunction was reversed by apocynin treatment. Moreover, apocynin prevented cellular oxidation [GSH/GSSG ratio: PSE APO rats vs. PSE rats in arbitrary units (au): 1.98 ± 0.07 vs. 1.35 ± 0.10; P < 0.001]. However, no differences in MDA were observed between groups. These data suggest that myocardial dysfunction observed after PSE was not due to β-adrenergic receptor desensitization but could be due to a signaling oxidative stress from the Nox enzyme. |
| Databáze: | OpenAIRE |
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