RESUMO
Stress is associated with cardiovascular disease. One accepted mechanism is autonomic imbalance. In this study, we investigated the effects of chronic mild stress (CMS) on cardiac autonomic control, cardiac structure and renin-angiotensin-aldosterone system (RAAS) activity in adult male Sprague Dawley rats. The CMS model provides a more realistic simulation of daily stress. The animals were divided into control and CMS, and were exposed to 4-week mild stressors. The electrocardiogram recording, sucrose intake and parameters related to stress, cardiac alterations and RAAS were determined. The results showed that CMS had lower body weight and higher sucrose intake. The heart rate variability (HRV) revealed that CMS increased autonomic activity without affecting its balance. The increased RAAS activity with upregulated angiotensin type 1 receptor mRNA expression was shown in CMS. The increased sympathetic activity or RAAS was correlated with stress. Moreover, the altered cardiac structure (i.e., heart weight and cardiomyocyte cross-sectional area) were correlated with stress-, sympathetic- and RAAS-related parameters. These indicated that CMS-induced cardiac hypertrophy was the result of both sympathetic and RAAS activation. Therefore, it could be concluded that 4-week CMS in male rats induced negative emotion as shown by increased sucrose intake, and increased cardiac autonomic and RAAS activities, which may be responsible for mild cardiac hypertrophy. The cardiac hypertrophy herein was possibly in an adaptive, not pathological, stage, and the cardiac autonomic function was preserved as the autonomic activities were in balance.
RESUMO
Stress is associated with cardiovascular diseases. One possible mechanism is the reduction in gamma-aminobutyric acid (GABA)ergic transmission at the paraventricular nucleus (PVN), which contributes to the disinhibition of sympathoexcitatory circuits and activates sympathetic outflow. At present, the mechanism of chronic mild stress (CMS) on GABAergic transmission at the PVN and cardiac autonomic activity is not yet fully clarified. Therefore, this study was designed to investigate the effects of CMS on the GABAergic system at the PVN and on the cardiac autonomic activity. Adult male Sprague-Dawley rats were randomly assigned to control (left undisturbed in their home cage) or CMS (subjected to various mild stressors for 4 weeks). Cardiac autonomic activities were determined by heart rate variability (HRV) analysis, and GABAergic alterations at the PVN were determined from GABA levels and mRNA expression of GABA-related activities. Results showed that the CMS group had decreased HRV as determined by the standard deviation of all R-R intervals (SDNN). The low frequency (LF) and high frequency (HF) powers of the CMS group were higher than those of the control. Hence, the LF/HF ratio was consequently unaffected. These findings indicated that despite the increase in sympathetic and parasympathetic activities, the autonomic balance was preserved at 4 weeks post CMS. For the GABAergic-related parameters, the CMS group had decreased mRNA expression of glutamic acid decarboxylase-65 (GAD-65), the GABA-synthesizing enzyme, and increased mRNA expression of gamma-aminobutyric acid transporter-1 (GAT-1). Moreover, the GAD-65 mRNA expression was negatively correlated with LF. In conclusion, 4-week CMS exposure in male rats could attenuate GABAergic transmission at the PVN and alter cardiac autonomic activities.
