title: Role of the renin-angiotensin system, renal sympathetic nerve system, and oxidative stress in chronic foot shock-induced hypertension in rats.
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.
authors.affiliation: 1. Department of Physiology and Neuroscience, Medical College of Soochow University, Suzhou 215123, P.R. China.
authors.forename: Tao
authors.initials: T
authors.lastname: Dong
authors.affiliation: 2. Department of Internal Medicine, the Affiliated Suzhou Chinese Traditional Medicine Hospital, Nanjing University of Chinese Medicine, Suzhou 215003, P.R. China.
authors.forename: Jing-Wei
authors.initials: JW
authors.lastname: Chen
authors.affiliation: 1. Department of Physiology and Neuroscience, Medical College of Soochow University, Suzhou 215123, P.R. China.
authors.forename: Li-Li
authors.initials: LL
authors.lastname: Tian
authors.affiliation: 1. Department of Physiology and Neuroscience, Medical College of Soochow University, Suzhou 215123, P.R. China.
authors.forename: Lin-Hui
authors.initials: LH
authors.lastname: Wang
authors.affiliation: 1. Department of Physiology and Neuroscience, Medical College of Soochow University, Suzhou 215123, P.R. China.
authors.forename: Ren-Di
authors.initials: RD
authors.lastname: Jiang
authors.affiliation: 1. Department of Physiology and Neuroscience, Medical College of Soochow University, Suzhou 215123, P.R. China.
authors.forename: Zhe
authors.initials: Z
authors.lastname: Zhang
authors.affiliation: 1. Department of Physiology and Neuroscience, Medical College of Soochow University, Suzhou 215123, P.R. China.
authors.forename: Jian-Bing
authors.initials: JB
authors.lastname: Xu
authors.affiliation: 2. Department of Internal Medicine, the Affiliated Suzhou Chinese Traditional Medicine Hospital, Nanjing University of Chinese Medicine, Suzhou 215003, P.R. China.
authors.forename: Xiao-Dong
authors.initials: XD
authors.lastname: Zhao
authors.affiliation: 3. Department of Internal Medicine, the Second Affiliated Hospital, High-tech zone hospital, Soochow University, Suzhou 215151, P.R. China.
authors.forename: Wei
authors.initials: W
authors.lastname: Zhu
authors.affiliation: 1. Department of Physiology and Neuroscience, Medical College of Soochow University, Suzhou 215123, P.R. China.
authors.forename: Guo-Qing
authors.initials: GQ
authors.lastname: Wang
authors.affiliation: 4. Laboratory of Molecular Diagnostics, Medical College of Soochow University, Suzhou 215123, P.R. China.
authors.forename: Wan-Ping
authors.initials: WP
authors.lastname: Sun
authors.affiliation: 1. Department of Physiology and Neuroscience, Medical College of Soochow University, Suzhou 215123, P.R. China.
authors.forename: Guo-Xing
authors.initials: GX
authors.lastname: Zhang
mesh_terms: D000804:Angiotensin II / Q000097:blood; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000378:metabolism / Q000494:pharmacology; D000808:Angiotensinogen / Q000378:metabolism; D000818:Animals; D002216:Captopril / Q000494:pharmacology; D003345:Corticosterone / Q000097:blood; D003497:Cyclic N-Oxides / Q000494:pharmacology; D003714:Denervation; D004558:Electric Stimulation; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D018384:Oxidative Stress; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D012083:Renin / Q000378:metabolism; D012084:Renin-Angiotensin System; D013113:Spin Labels; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D003497:Cyclic N-Oxides; D044140:Receptor, Angiotensin, Type 1; D013113:Spin Labels; D017392:Thiobarbituric Acid Reactive Substances; D000808:Angiotensinogen; D000804:Angiotensin II; D002216:Captopril; D012083:Renin; C001803:tempol; D003345:Corticosterone
keywords: foot shock; hypertension; oxidative stress; renal sympathetic nerve denervation; renin-angiotensin system (RAS)