title: Angiotensin II and AT1 receptor in hypertrophied ventricles and aortas of sinoaortic-denervated rats.
abstract: OBJECTIVE
  Angiotensin II and AT1 receptor are the major effector components of renin-angiotensin system (RAS), and also the main growth-stimulating factors in cardiovascular system. The present study was to observe these two factors in the hypertrophied ventricles and aortas of sinoaortic-denervated rats.
  
  
  METHODS
  Rats were examined at 2, 10, and 16 weeks after sinoaortic denervation (SAD). The hypertrophy was evaluated by the ratio of organ weight to body weight. Angiotensin II concentration and AT1 receptor mRNA expression were measured by radioimmunoassay and RT-PCR respectively, using a positive control of candesartan treatment.
  
  
  RESULTS
  Aortic hypertrophy existed in 2-, 10-, and 16-week SAD rats, left ventricular hypertrophy in 10- and 16-week SAD rats, and right ventricular hypertrophy in 16-week SAD rats. In all three kinds of examined SAD rats, plasma angiotensin II levels remained unchanged, indicating circulating RAS is at normal level in the chronic phase of SAD. However, cardiovascular tissue RAS was activated, as evidenced by increase of aortic angiotensin II concentrations at 10 and 16 weeks after SAD, and up-regulation of aortic and left ventricular AT1 receptor mRNA expressions at 16 weeks after SAD.
  
  
  CONCLUSIONS
  The activated tissue RAS is secondary to the hypertrophy, and probably involved in the maintenance of cardiovascular hypertrophy following SAD.
authors.affiliation: Department of Pharmacology, Basic Medical College, Second Military Medical University, Shanghai 200433, China. cymiao@citiz.net
authors.forename: Chao-Yu
authors.initials: CY
authors.lastname: Miao
authors.forename: Li-Ming
authors.initials: LM
authors.lastname: Zhang
authors.forename: Wen-Jun
authors.initials: WJ
authors.lastname: Yuan
authors.forename: Ding-Feng
authors.initials: DF
authors.lastname: Su
mesh_terms: D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D001011:Aorta / Q000378:metabolism / Q000473:pathology; D003714:Denervation; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology; D006984:Hypertrophy; D017379:Hypertrophy, Left Ventricular / Q000378:metabolism* / Q000473:pathology; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000096:biosynthesis* / Q000235:genetics; D012084:Renin-Angiotensin System / Q000502:physiology; D012849:Sinoatrial Node / Q000294:innervation*
chemical_list: D012333:RNA, Messenger; D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II