Exercise training reduces sympathetic modulation on cardiovascular system and cardiac oxidative stress in spontaneously hypertensive rats.
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.
Bertagnolli
Mariane
M
Laboratory of Cardiovascular Physiology, Department of Physiology, Basic and Health Science Institute, Federal University of Rio Grande do Sul, Porto Alegre, Brazil.
Schenkel
Paulo C
PC
Campos
Cristina
C
Mostarda
Cristiano T
CT
Casarini
Dulce E
DE
Belló-Klein
Adriane
A
Irigoyen
Maria C
MC
Rigatto
Katya
K
D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002320:Cardiovascular Physiological Phenomena; D002319:Cardiovascular System / Q000294:innervation*; D006321:Heart / Q000502:physiology*; D006352:Heart Ventricles / Q000473:pathology; D006973:Hypertension / Q000503:physiopathology* / Q000517:prevention & control*; D006984:Hypertrophy / Q000503:physiopathology / Q000517:prevention & control; D015227:Lipid Peroxidation / Q000502:physiology; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D013564:Sympathetic Nervous System / Q000502:physiology*
D009569:Nitric Oxide; D009638:Norepinephrine