| Exercise training reduces sympathetic modulation on cardiovascular system and cardiac oxidative stress in spontaneously hypertensive rats. | |
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MedLine Citation:
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PMID: 18787517 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Spontaneously hypertensive rats (SHRs) show increased cardiac sympathetic activity, which could stimulate cardiomyocyte hypertrophy, cardiac damage, and apoptosis. Norepinephrine (NE)-induced cardiac oxidative stress seems to be involved in SHR cardiac hypertrophy development. Because exercise training (ET) decreases sympathetic activation and oxidative stress, it may alter cardiac hypertrophy in SHR. The aim of this study was to determine, in vivo, whether ET alters cardiac sympathetic modulation on cardiovascular system and whether a correlation exists between cardiac oxidative stress and hypertrophy. METHODS: Male SHRs (15-weeks old) were divided into sedentary hypertensive (SHR, n = 7) and exercise-trained hypertensive rats (SHR-T, n = 7). Moderate ET was performed on a treadmill (5 days/week, 60 min, 10 weeks). After ET, cardiopulmonary reflex responses were assessed by bolus injections of 5-HT. Autoregressive spectral estimation was performed for systolic arterial pressure (SAP) with oscillatory components quantified as low (LF: 0.2-0.75 Hz) and high (HF: 0.75-4.0 Hz) frequency ranges. Cardiac NE concentration, lipid peroxidation, antioxidant enzymes activities, and total nitrates/nitrites were determined. RESULTS: ET reduced mean arterial pressure, SAP variability (SAP var), LF of SAP, and cardiac hypertrophy and increased cardiopulmonary reflex responses. Cardiac lipid peroxidation was decreased in trained SHRs and positively correlated with NE concentrations (r = 0.89, P < 0.01) and heart weight/body weight ratio (r = 0.72, P < 0.01), and inversely correlated with total nitrates/nitrites (r = -0.79, P < 0.01). Moreover, in trained SHR, cardiac total nitrates/nitrites were inversely correlated with NE concentrations (r = -0.82, P < 0.01). CONCLUSIONS: ET attenuates cardiac sympathetic modulation and cardiac hypertrophy, which were associated with reduced oxidative stress and increased nitric oxide (NO) bioavailability. |
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Authors:
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Mariane Bertagnolli; Paulo C Schenkel; Cristina Campos; Cristiano T Mostarda; Dulce E Casarini; Adriane Belló-Klein; Maria C Irigoyen; Katya Rigatto |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2008-09-11 |
Journal Detail:
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Title: American journal of hypertension Volume: 21 ISSN: 1941-7225 ISO Abbreviation: Am. J. Hypertens. Publication Date: 2008 Nov |
Date Detail:
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Created Date: 2008-10-22 Completed Date: 2009-01-30 Revised Date: 2011-06-30 |
Medline Journal Info:
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Nlm Unique ID: 8803676 Medline TA: Am J Hypertens Country: United States |
Other Details:
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Languages: eng Pagination: 1188-93 Citation Subset: IM |
Affiliation:
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Laboratory of Cardiovascular Physiology, Department of Physiology, Basic and Health Science Institute, Federal University of Rio Grande do Sul, Porto Alegre, Brazil. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Pressure / physiology Cardiovascular Physiological Phenomena Cardiovascular System / innervation* Heart / physiology* Heart Ventricles / pathology Hypertension / physiopathology*, prevention & control* Hypertrophy / physiopathology, prevention & control Lipid Peroxidation / physiology Male Nitric Oxide / metabolism Norepinephrine / metabolism Oxidative Stress / physiology* Physical Conditioning, Animal / physiology* Rats Rats, Inbred SHR Sympathetic Nervous System / physiology* |
| Chemical | |
Reg. No./Substance:
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10102-43-9/Nitric Oxide; 51-41-2/Norepinephrine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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