title: [Inhibitory effect on activated renin-angiotensin system by astragaloside IV in rats with pressure-overload induced cardiac hypertrophy].
abstract: OBJECTIVE
  To investigate the effect of astragaloside IV (As IV) on the activation of rennin-angiotensin system in rats with pressure-overload induced cardiac hypertrophy.
  
  
  METHODS
  Left ventricle hypertrophy was induced by abdominal aorta banding between bilateral renal aortas for 12 weeks. Rats were given astragaloside IV 1.0 mg x kg(-1) and 3.3 mg x kg(-1) for 12 weeks, respectively. After treatment, the left ventricular mass index (LVMI)was calculated by morphometry methods. Plasma and cardiac tissue angiotensin II, and plasma aldosterone were measured by ELISA method. Gene expressions of ACE, AT1 and AT2 in cardiac tissue were detected by real time PCR. Protein expressions of AT1 and AT2 in cardiac tissue were detected by Western blot.
  
  
  RESULTS
  Compared with model rats, LVMI was decreased by astragaloside IV treatment. Biochemical results indicated that the contents of angiotensin II in plasma and cardiac tissue as well as aldosterone in plasma were all increased in abdominal aorta banding rats comparing with sham-operated rats, then, decreased by astragaloside IV treatment. Gene expressions of cardiac ACE was downregulated by astragaloside IV, however, gene and protein expressions of cardiac AT2 were upregulated by astragaloside IV. Both elevated gene and protein expressions of AT1 were not attenuated by astragaloside IV.
  
  
  CONCLUSIONS
  Excessive activated rennin-angiotensin system in rats with pressure-overload induced cardiac hypertrophy is inhibited by astragaloside IV treatment.
authors.affiliation: Institute of Materia Medica, Shanghai University of Tradition Chinese Medicine, Shanghai 201203, China.
authors.forename: Hailian
authors.initials: H
authors.lastname: Shi
authors.forename: Chunlai
authors.initials: C
authors.lastname: Ma
authors.forename: Yan
authors.initials: Y
authors.lastname: Liu
authors.forename: Jiyan
authors.initials: J
authors.lastname: Zhou
authors.forename: Zhibi
authors.initials: Z
authors.lastname: Hu
authors.forename: Dazheng
authors.initials: D
authors.lastname: Wu
mesh_terms: D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000097:blood / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D006332:Cardiomegaly / Q000188:drug therapy*; D004797:Enzyme-Linked Immunosorbent Assay; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy / Q000378:metabolism; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics; D016133:Polymerase Chain Reaction; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics; D044139:Receptor, Angiotensin, Type 2 / Q000235:genetics; D012084:Renin-Angiotensin System / Q000187:drug effects*; D012503:Saponins / Q000627:therapeutic use*; D014315:Triterpenes / Q000627:therapeutic use*
chemical_list: D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D012503:Saponins; D014315:Triterpenes; D000804:Angiotensin II; C052064:astragaloside A; D000450:Aldosterone; D007703:Peptidyl-Dipeptidase A