Chinese Journal of Tissue Engineering Research ›› 2022, Vol. 26 ›› Issue (14): 2231-2237.doi: 10.12307/2022.488

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Regulatory mechanism of aerobic exercise on cardiac remodeling in spontaneously hypertensive rats

Zhu Zheng1, Fu Changxi1, Ma Wenchao1, Ma Gang2, Peng peng2   

  1. 1Department of Physical Education, Xuzhou University of Technology, Xuzhou 221018, Jiangsu Province, China; 2Department of Health Service, Logistics University of Chinese People’s Armed Police Forces, Tianjin 300309, China
  • Received:2021-06-03 Revised:2021-06-23 Accepted:2021-07-01 Online:2022-05-18 Published:2021-12-22
  • Contact: Peng Peng, MD, Lecturer, Department of Health Service, Logistics University of Chinese People’s Armed Police Forces, Tianjin 300309, China
  • About author:Zhu Zheng, Master, Lecturer, Department of Physical Education, Xuzhou University of Technology, Xuzhou 221018, Jiangsu Province, China
  • Supported by:
    the Natural Science Foundation of Tianjin, No. 17JCYBJC27400 (to PP)

Abstract: BACKGROUND: Renin-angiotensin system is the main pathophysiological mechanism that mediates the occurrence and development of hypertension. Regular exercise, especially aerobic exercise, can prevent and treat many cardiovascular diseases. However, the optimal exercise prescription for hypertension has not been determined.
OBJECTIVE: To observe the effect of aerobic exercise on cardiac remodeling and to investigate the possible mechanism of local and systemic renin-angiotensin system in spontaneously hypertensive rats (SHR)
METHODS: Thirty male SHR rats were randomly divided into SHR sedentary group and SHR exercise group. At the same time, 15 Wistar-Kyoto rats were used as normal blood pressure control group (WKY). The animals in the WKY and SHR sedentary groups were caged and raised quietly, and the SHR exercise group performed moderate intensity treadmill exercise for 8 weeks. After the experiment, caudal artery blood pressure was measured by non-invasive sphygmomanometer. Cardiac structure and function were detected by echocardiography. Myocardial histopathology was observed by hematoxylin-eosin and Masson staining. Angiotensin converting enzyme (ACE) and ACE2 activities in serum and heart were measured by fluorescence substrate method, and angiotensin II (Ang II) and Ang(1-7) contents in serum and heart were detected by high performance liquid chromatography. The protein expression of ACE, Ang II type 1 receptor (AT1R), ACE2 and Mas receptor was detected by western blot. The study protocol was reviewed and approved by the Ethics Committee of Xuzhou University of Technology (approval No. XZUTLL 2019-003-02).
RESULTS AND CONCLUSION: Cardiac structure and function: compared with the WKY group, blood pressure increased (P < 0.05), left ventricular concentric hypertrophy and myocardial fibrosis occurred (P < 0.05), and cardiac function decreased (P < 0.05) in SHR sedentary group. Compared with the SHR sedentary group, blood pressure decreased (P < 0.05), left ventricle presented eccentric hypertrophy and myocardial fibrosis alleviated (P < 0.05), and cardiac function improved (P < 0.05) in the SHR exercise group. Local (heart) renin-angiotensin system: compared with the SHR sedentary group, cardiac ACE activity and protein expression and Ang II content decreased (P < 0.05), Ang(1-7) content increased (P < 0.05), ACE2 and Mas receptor protein expression upregulated (P < 0.05), ACE/ACE2 activity and protein expression ratio, Ang II/Ang(1-7) content ratio, and AT1R/Mas receptor protein expression ratio decreased (P < 0.05) in the SHR exercise group. Systemic renin-angiotensin system: there was no significant difference in the activity of ACE and ACE2, ACE/ACE2 activity ratio, the content of Ang II and Ang(1-7), and Ang II/Ang(1–7) content ratio of serum in all groups (P > 0.05). To conclude, aerobic exercise regulates local (heart) renin-angiotensin system to shift ACE-Ang II-AT1R axis to ACE2-Ang(1-7)-Mas receptor axis, thereby inhibiting cardiac remodeling in SHR rats.

Key words: aerobic exercise, hypertension, renin-angiotensin system, cardiac remodeling, heart failure

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