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Int J Biol Sci 2015; 11(6):652-663. doi:10.7150/ijbs.10250

Research Paper

Role of the Renin-Angiotensin System, Renal Sympathetic Nerve System, and Oxidative Stress in Chronic Foot Shock-Induced Hypertension in Rats

Tao Dong1, *, Jing-Wei Chen2, *, Li-Li Tian1, *, Lin-Hui Wang1, Ren-Di Jiang1, Zhe Zhang1, Jian-Bing Xu1, Xiao-Dong Zhao2, Wei Zhu3, Guo-Qing Wang1, Wan-Ping Sun4, ✉, Guo-Xing Zhang1, ✉

1. Department of Physiology and Neuroscience, Medical College of Soochow University, Suzhou 215123, P.R. China
2. Department of Internal Medicine, the Affiliated Suzhou Chinese Traditional Medicine Hospital, Nanjing University of Chinese Medicine, Suzhou 215003, P.R. China
3. Department of Internal Medicine, the Second Affiliated Hospital, High-tech zone hospital, Soochow University, Suzhou 215151, P.R. China
4. Laboratory of Molecular Diagnostics, Medical College of Soochow University, Suzhou 215123, P.R. China
* These authors contributed equally to this work.

Abstract

Objective: The renin-angiotensin system (RAS) and renal sympathetic nerve system (RSNS) are involved in the development of hypertension. The present study is designed to explore the possible roles of the RAS and the RSNS in foot shock-induced hypertension.

Methods: Male Sprague-Dawley rats were divided into six groups: control, foot shock, RSNS denervation, denervation plus foot shock, Captopril (angiotensin I converting enzyme inhibitor, ACE inhibitor) plus foot shock, and Tempol (superoxide dismutase mimetic) plus foot shock. Rats received foot shock for 14 days. We measured the quantity of thiobarbituric acid reactive substances (TBARS), corticosterone, renin, and angiotensin II (Ang II) in plasma, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and renal noradrenaline content. RAS component mRNA and protein levels were quantified in the cerebral cortex and hypothalamus.

Results: The two week foot shock treatment significantly increased systolic blood pressure, which was accompanied by an increase in angiotensinogen, renin, ACE1, and AT1a mRNA and protein expression in the cerebral cortex and hypothalamus, an increase of the plasma concentrations of renin, Ang II, corticosterone, and TBARS, as well as a decrease in plasma SOD and GSH-Px activities. Systolic blood pressure increase was suppressed by denervation of the RSNS or treatment with Captopril or Tempol. Interestingly, denervation or Tempol treatment both decreased main RAS components not only in the circulatory system, but also in the central nervous system. In addition, decreased antioxidant levels and increased TBARS and corticosterone levels were also partially restored by denervation or treatment with Tempol or Captopril.

Conclusions: RAS, RSNS and oxidative stress reciprocally potentiate to play important roles in the development of foot shock-induced hypertension.

Keywords: renal sympathetic nerve denervation, foot shock, hypertension, renin-angiotensin system (RAS), oxidative stress

This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) License. See http://ivyspring.com/terms for full terms and conditions.
How to cite this article:
Dong T, Chen JW, Tian LL, Wang LH, Jiang RD, Zhang Z, Xu JB, Zhao XD, Zhu W, Wang GQ, Sun WP, Zhang GX. Role of the Renin-Angiotensin System, Renal Sympathetic Nerve System, and Oxidative Stress in Chronic Foot Shock-Induced Hypertension in Rats. Int J Biol Sci 2015; 11(6):652-663. doi:10.7150/ijbs.10250. Available from http://www.ijbs.com/v11p0652.htm