Bangsumruaj Janpen, Kijtawornrat Anusak, Kalandakanond-Thongsong Sarinee
Interdisciplinary Program in Physiology, Graduate School, Chulalongkorn University, Bangkok 10330, Thailand.
Department of Veterinary Physiology, Faculty of Veterinary Science, Chulalongkorn University, Bangkok 10330, Thailand.
Vet Sci. 2022 Sep 29;9(10):539. doi: 10.3390/vetsci9100539.
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.
压力与心血管疾病有关。一种公认的机制是自主神经失衡。在本研究中，我们调查了慢性轻度应激（CMS）对成年雄性Sprague Dawley大鼠心脏自主神经控制、心脏结构和肾素-血管紧张素-醛固酮系统（RAAS）活性的影响。CMS模型能更真实地模拟日常应激。将动物分为对照组和CMS组，并使其暴露于为期4周的轻度应激源中。测定心电图记录、蔗糖摄入量以及与应激、心脏改变和RAAS相关的参数。结果显示，CMS组体重较低，蔗糖摄入量较高。心率变异性（HRV）表明，CMS增加了自主神经活动，但未影响其平衡。CMS组显示RAAS活性增加，1型血管紧张素受体mRNA表达上调。交感神经活动或RAAS的增加与应激相关。此外，心脏结构的改变（即心脏重量和心肌细胞横截面积）与应激、交感神经和RAAS相关参数相关。这些表明，CMS诱导的心脏肥大是交感神经和RAAS激活的结果。因此，可以得出结论，雄性大鼠4周的CMS诱导了如蔗糖摄入量增加所示的负面情绪，并增加了心脏自主神经和RAAS活性，这可能是轻度心脏肥大的原因。此处的心脏肥大可能处于适应性而非病理性阶段，并且由于自主神经活动处于平衡状态，心脏自主神经功能得以保留。
