title: [Research on Rho-kinase expression in pulmonary arterioles of rat exposed to hypoxia].
abstract: OBJECTIVE
  To evaluate the expression and the role of Rho-kinase (ROCK I and ROCK II )in the development of hypoxic pulmonary hypertension of rat.
  
  
  METHODS
  Thirty six of adult male SD rats were randomly divided into six groups; one group was exposed to air as normal control, the other five groups were exposed to isobaric hypoxia for 1 day, 3 days, 1 week, 2 weeks and 3 weeks respectively. Microtube method was used to measure the mean pulmonary arterial pressure (mPAP). The right ventricle (RV) and left ventricle plus atrial ventricular septum (LV+S) were isolated and weighed to calculate the value of RV/(LV+S). The amounts of Rho-kinase and Rho-kinase mRNA in rat pulmonary artery were determined by immunohistochemistry, in situ hybridization and image analysis.
  
  
  RESULTS
  The mPAP and RV/(LV+S) values increased with time prolongation of rats exposed to hypoxia (P<0.05). The ratio of arteriole wall thickness/vascular external diameter(WT%) and vascular area/total vascular area(WA%) went forward to a height with exposing rats to hypoxia for a long time; WT% and WA% of hypoxia group rats exposed for 3 weeks were significantly higher than that of control group (P<0.05). All of ROCK I , ROCK II, ROCK I mRNA and ROCK II mRNA in pulmonary arterioles got the enhanced positive signals of immunohistochemistry staining or in situ hybridization with prolonging the time of rats exposed to hypoxia. The hypoxia group for 3 weeks got significantly stronger staining signals of Rho-kinase and Rho-kinase mRNA in pulmonary arterioles than that of control group (P<0.05). The positive staining of ROCK I , ROCK I mRNA, ROCK II or ROCK II mRNA in pulmonary arterioles all positively related with mPAP, WA% and WT% (r=0.404, 0.267 and 0.263; 0.500, 0.263 and 0.260; 0.490, 0.295 and 0.286; 0.579, 0.251 and 0.254) (P<0.05).
  
  
  CONCLUSIONS
  Hypoxia led Rho-kinase and Rho-kinase mRNA to have an increased expression. Rho-kinase may play a role in the development of hypoxic pulmonary hypertension by contracting and remodeling pulmonary arterioles.
authors.affiliation: Department of Respiratory, West China Hospital, Sichuan University, Chengdu 610041, China.
authors.forename: Li
authors.initials: L
authors.lastname: Yang
authors.forename: De-yun
authors.initials: DY
authors.lastname: Cheng
authors.forename: Xiao-ju
authors.initials: XJ
authors.lastname: Chen
authors.forename: Oiao-li
authors.initials: OL
authors.lastname: Su
authors.forename: Xiu-qiong
authors.initials: XQ
authors.lastname: Xia
mesh_terms: D000818:Animals; D001160:Arterioles / Q000378:metabolism; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000378:metabolism*; D000860:Hypoxia / Q000150:complications*; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics; D008297:Male; D017346:Protein Serine-Threonine Kinases / Q000096:biosynthesis* / Q000235:genetics; D011651:Pulmonary Artery / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D054460:rho-Associated Kinases
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; D012333:RNA, Messenger; D017346:Protein Serine-Threonine Kinases; D054460:rho-Associated Kinases