title: [Blockade of renin-angiotensin system attenuates cardiac remodeling in rats undergoing aortic stenosis].
abstract: OBJECTIVE
  To assess the role of the AT1 receptor blocker and the angiotensin-converting enzyme inhibitor in cardiac remodeling induced by aortic stenosis in rats.
  
  
  METHODS
  Wistar rats were divided into the following 4 groups: 1) C--control (n=13); 2) AoS--aortic stenosis (n=11); 3) LIS--AoS treated with lisinopril, 20 mg/kg/day (n=11); and 4) LOS--AoS treated with losartan, 40 mg/kg/day (n=9). The treatments were initiated 3 days before surgery. After 6 weeks, the animals underwent echocardiographic study, and quantification of the hydroxyproline (HOP) concentration and the left ventricular (LV) myocyte cross-sectional area (CSA).
  
  
  RESULTS
  Aortic stenosis induced an increase in left ventricular wall thickness. The LIS and LOS groups showed no difference as compared with the control group. The AoS and LIS rats had greater left atrial diameters than the control rats did, while no difference was observed in the LOS animals. The AoS animals had greater values of shortening percentage than control animals did. This fact was modified with neither LIS nor LOS. The cross-sectional area of the animals in the AoS group was greater than that in the control group. However, treatment with LOS and LIS attenuated the AoS-induced increase in area. Aortic stenosis caused an increase in HOP concentration, while the LOS group showed no difference as compared with the control group.
  
  
  CONCLUSIONS
  Blockade of the renin-angiotensin system with AT1 blocker and ACEI may attenuate the development of heart hypertrophy, but only the blockade of AT1 receptors attenuates left ventricular interstitial fibrosis.
authors.affiliation: Faculdade de Medicina de Botucatu, UNESP, Botucatu, SP.
authors.forename: Giancarlo
authors.initials: G
authors.lastname: Gonçalves
authors.forename: Leonardo A M
authors.initials: LA
authors.lastname: Zornoff
authors.forename: Henrique B
authors.initials: HB
authors.lastname: Ribeiro
authors.forename: Marina P
authors.initials: MP
authors.lastname: Okoshi
authors.forename: Fernando R S
authors.initials: FR
authors.lastname: Cordaro
authors.forename: Katashi
authors.initials: K
authors.lastname: Okoshi
authors.forename: Carlos R
authors.initials: CR
authors.lastname: Padovani
authors.forename: Flávio F
authors.initials: FF
authors.lastname: Aragon
authors.forename: Antonio C
authors.initials: AC
authors.lastname: Cicogna
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D001024:Aortic Valve Stenosis / Q000150:complications*; D004452:Echocardiography; D006909:Hydroxyproline / Q000032:analysis; D017379:Hypertrophy, Left Ventricular / Q000517:prevention & control*; D017706:Lisinopril / Q000494:pharmacology*; D019808:Losartan / Q000494:pharmacology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D020257:Ventricular Remodeling / Q000187:drug effects*
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D017706:Lisinopril; D019808:Losartan; D006909:Hydroxyproline