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Aerobic exercise inhibits sympathetic nerve sprouting and restores ?-adrenergic receptor balance in rats with myocardial infarction.

ABSTRACT:

Background

Cardiac sympathetic nerve sprouting and the dysregulation of ?-adrenergic receptor (?-AR) play a critical role in the deterioration of cardiac function after myocardial infarction (MI). Growing evidence indicates that exercise provides protection against MI. The aims of this study were to investigate whether aerobic exercise following MI could inhibit sympathetic nerve sprouting and restore the balance of ?3-AR/?1-AR.

Methods

Male Sprague-Dawley rats were divided into three groups: sham-operated control group (SC), MI group (MI), and MI with aerobic exercise group (ME). The rats in ME group were assigned to 8 weeks of exercise protocol (16 m/min, 50 min/d, 5 d/wk). The expression of nerve growth factor (NGF), the sympathetic nerve marker-tyrosine hydroxylase (TH), the nerve sprouting marker-growth associated protein 43 (GAP43), and ?1- and ?2-AR expression in the peri-infarct area of the left ventricle (LV) were measured by Western blot and immunohistochemistry, while ?3-AR expression was determined by Western blot and immunofluorescence. Endothelial nitric oxide synthase (NOS2), phospho-NOS2 (p-NOS2), and neuronal nitric oxide synthase (NOS1) were measured by Western blot.

Results

MI increased LV end-diastolic pressure (LVEDP), and decreased LV systolic pressure (LVSP). Compared with the MI group, aerobic exercise significantly decreased LVEDP and increased LVSP. The protein expression of TH, GAP43 and NGF was significantly increased after MI, which was normalized by exercise. Compared with the SC group, the ratios of ?2-AR/?1-AR and ?3-AR/?1-AR were elevated in the MI group, and the protein expression of ?3-AR and NOS1 increased after MI. Compared with the MI group, the ratios of ?2-AR/?1-AR and ?3-AR/?1-AR were normalized in the ME group, while the protein expression of ?3-AR and NOS1 significantly increased, and NOS2 was activated by exercise.

Conclusions

Aerobic exercise inhibits cardiac sympathetic nerve sprouting, restores ?3-AR/?1-AR balance and increases ?3-AR expression through the activation of NOS2 and NOS1 after myocardial infarction.

SUBMITTER: Chen T

PROVIDER: S-EPMC4026473 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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Publications

Aerobic exercise inhibits sympathetic nerve sprouting and restores β-adrenergic receptor balance in rats with myocardial infarction.

Chen Ting T Cai Meng-Xin MX Li You-You YY He Zhi-Xiong ZX Shi Xiu-Chao XC Song Wei W Wang You-Hua YH Xi Yue Y Kang Yu-Ming YM Tian Zhen-Jun ZJ

PloS one 20140519 5

<h4>Background</h4>Cardiac sympathetic nerve sprouting and the dysregulation of β-adrenergic receptor (β-AR) play a critical role in the deterioration of cardiac function after myocardial infarction (MI). Growing evidence indicates that exercise provides protection against MI. The aims of this study were to investigate whether aerobic exercise following MI could inhibit sympathetic nerve sprouting and restore the balance of β3-AR/β1-AR.<h4>Methods</h4>Male Sprague-Dawley rats were divided into t ...[more]

PMID: 24842290

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