title: Renin angiotensin system and cardiac hypertrophy after sinoaortic denervation in rats.
abstract: OBJECTIVE
  The aim of this study was to evaluate the role of angiotensin I, II and 1-7 on left ventricular hypertrophy of Wistar and spontaneously hypertensive rats submitted to sinoaortic denervation.
  
  
  METHODS
  Ten weeks after sinoaortic denervation, hemodynamic and morphofunctional parameters were analyzed, and the left ventricle was dissected for biochemical analyses.
  
  
  RESULTS
  Hypertensive groups (controls and denervated) showed an increase on mean blood pressure compared with normotensive ones (controls and denervated). Blood pressure variability was higher in denervated groups than in their respective controls. Left ventricular mass and collagen content were increased in the normotensive denervated and in both spontaneously hypertensive groups compared with Wistar controls. Both hypertensive groups presented a higher concentration of angiotensin II than Wistar controls, whereas angiotensin 1-7 concentration was decreased in the hypertensive denervated group in relation to the Wistar groups. There was no difference in angiotensin I concentration among groups.
  
  
  CONCLUSIONS
  Our results suggest that not only blood pressure variability and reduced baroreflex sensitivity but also elevated levels of angiotensin II and a reduced concentration of angiotensin 1-7 may contribute to the development of left ventricular hypertrophy. These data indicate that baroreflex dysfunction associated with changes in the renin angiotensin system may be predictive factors of left ventricular hypertrophy and cardiac failure.
authors.affiliation: Heart Institute, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil. hipirigoyen@incor.usp.br
authors.forename: Aline Cristina
authors.initials: AC
authors.lastname: Piratello
authors.forename: Ivana
authors.initials: I
authors.lastname: Moraes-Silva
authors.forename: Janaina
authors.initials: J
authors.lastname: Paulini
authors.forename: Pamella Ramona
authors.initials: PR
authors.lastname: Souza
authors.forename: Raquel
authors.initials: R
authors.lastname: Sirvente
authors.forename: Vera
authors.initials: V
authors.lastname: Salemi
authors.forename: Karin
authors.initials: K
authors.lastname: Flues
authors.forename: Edson Dias
authors.initials: ED
authors.lastname: Moreira
authors.forename: Cristiano
authors.initials: C
authors.lastname: Mostarda
authors.forename: Tatiana
authors.initials: T
authors.lastname: Cunha
authors.forename: Dulce Elena
authors.initials: DE
authors.lastname: Casarini
authors.forename: Maria Claudia
authors.initials: MC
authors.lastname: Irigoyen
mesh_terms: D000803:Angiotensin I / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002346:Carotid Sinus / Q000294:innervation*; D003094:Collagen / Q000032:analysis; D003714:Denervation; D004195:Disease Models, Animal; D006352:Heart Ventricles / Q000473:pathology*; D006439:Hemodynamics / Q000502:physiology; D006973:Hypertension / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000473:pathology*; D008297:Male; D010446:Peptide Fragments / Q000097:blood; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012084:Renin-Angiotensin System / Q000502:physiology*
chemical_list: D010446:Peptide Fragments; D000804:Angiotensin II; D003094:Collagen; D000803:Angiotensin I; C118790:angiotensin I (1-7)