title: Activation of renin-angiotensin-aldosterone system (RAAS) in the lung of smoking-induced pulmonary arterial hypertension (PAH) rats.
abstract: OBJECTIVE
  To explore the role of the renin-angiotensin-aldosterone system (RAAS) in the pathogenesis of pulmonary arterial hypertension (PAH) induced by chronic exposure to cigarette smoke.
  
  
  METHODS
  48 healthy male SD rats were randomly divided into four groups (12/group): control group (group A); inhibitor alone group (group B); cigarette induction group (group C); cigarette induction + inhibitor group (group D). After the establishment of smoking-induced PAH rat model, the right ventricular systolic pressure (RVSP) was detected using an inserted catheter; western blotting was used to detect the protein expression of angiotensin-converting enzyme-2 (ACE2) and angiotensin-converting enzyme (ACE); expression levels of angiotensin II (AngII) in lung tissue were measured by radioimmunoassay.
  
  
  RESULTS
  After six months of cigarette exposure, the RVSP of chronic cigarette induction group was significantly higher than that of the control group; expression levels of AngII and ACE increased in lung tissues, but ACE2 expression levels reduced. Compared with cigarette exposure group, after losartan treatment, RVSP, ACE and AngII obviously decreased (P<0.05), and ACE2 expression levels significantly increased.
  
  
  CONCLUSIONS
  Chronic cigarette exposure may result in PAH and affect the protein expression of ACE2 and ACE in lung tissue, suggesting that ACE2 and ACE play an important role in the pathogenesis of smoking-induced PAH.
authors: Department of Geriatric Medicine, West China Hospital, Sichuan University, China yym28tb@163.com.
authors: Yi-Ming
authors: YM
authors: Yuan
authors: Department of Geriatric Medicine, West China Hospital, Sichuan University, China.
authors: Li
authors: L
authors: Luo
authors: ENT Department, Pixian TCM Hospital, China.
authors: Zhen
authors: Z
authors: Guo
authors: Department of Geriatric Medicine, West China Hospital, Sichuan University, China.
authors: Ming
authors: M
authors: Yang
authors: Department of Internal Medicine, The Affiliated Shanghai Eighth People's Hospital of Jiangsu University,Shanghai, China.
authors: Ren-Song
authors: RS
authors: Ye
authors: Department of Geriatric Medicine, West China Hospital, Sichuan University, China.
authors: Chuan
authors: C
authors: Luo
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D000085962:Angiotensin-Converting Enzyme 2; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D015153:Blotting, Western; D006352:Heart Ventricles / Q000187:drug effects / Q000503:physiopathology; D006976:Hypertension, Pulmonary / Q000188:drug therapy / Q000201:enzymology / Q000378:metabolism* / Q000503:physiopathology; D019808:Losartan / Q000494:pharmacology / Q000627:therapeutic use; D008168:Lung / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D012084:Renin-Angiotensin System / Q000187:drug effects; D012907:Smoking; D013599:Systole / Q000187:drug effects
chemical_list: D000804:Angiotensin II; D007703:Peptidyl-Dipeptidase A; C000705329:Ace2 protein, rat; D000085962:Angiotensin-Converting Enzyme 2; D019808:Losartan
keywords: PAH; RAAS; Smoking; chronic obstructive pulmonary disease