title: Expression of angiotensin II receptors in human left and right atrial tissue in atrial fibrillation with and without underlying mitral valve disease.
abstract: TIVES: We postulated a change of angiotensin II receptor subtype expression in patients with lone atrial fibrillation (AF) and AF with underlying mitral valve disease (MVD) both compared with sinus rhythm (SR).
  
  
  BACKGROUND
  Atrial fibrillation is a progressive disease associated with electrical and structural remodeling. Angiotensin II (ANGII) is involved in the process of myocardial remodeling. Actions of ANGII are mediated by ANGII receptor subtypes 1 and 2 (AT(1) and AT(2)).
  
  
  METHODS
  Left atrial (LA) and right atrial (RA) tissue samples were obtained from patients with AF or SR with or without underlying MVD. The AT(1) and AT(2) protein levels were measured by quantitative Western blotting techniques.
  
  
  RESULTS
  The AT(1) protein level in the LA was significantly increased in patients with AF (all forms) compared with SR (p < 0.05), whereas AT(2) expression was not significantly altered. Comparison of the subgroups revealed a similar increase of AT(1) in both paroxysmal AF and chronic AF with or without MVD. Additionally, investigations of ANGII receptor subtypes in the RA did not exhibit any significant changes either in AT(1) or in AT(2) in patients with AF versus SR. Underlying MVD did not significantly affect AT(2) receptor subtype expression in LA.
  
  
  CONCLUSIONS
  Atrial fibrillation is associated with an up-regulation of AT(1) in LA, but not in RA, and did not appear to influence the AT(2) expression in the atrium. Because we found an enhanced expression of AT(1)in the LA, we conclude that AT(1) might be involved in the pathogenesis of AF in the LA.
authors.affiliation: University of Leipzig, Heart Center, Cardiovascular Surgery, Cardiology, Leipzig, Germany. Andreas.Boldt@web.de
authors.forename: Andreas
authors.initials: A
authors.lastname: Boldt
authors.forename: Ulrike
authors.initials: U
authors.lastname: Wetzel
authors.forename: Josef
authors.initials: J
authors.lastname: Weigl
authors.forename: Jens
authors.initials: J
authors.lastname: Garbade
authors.forename: Jörg
authors.initials: J
authors.lastname: Lauschke
authors.forename: Gerhard
authors.initials: G
authors.lastname: Hindricks
authors.forename: Hans
authors.initials: H
authors.lastname: Kottkamp
authors.forename: Jan Fritz
authors.initials: JF
authors.lastname: Gummert
authors.forename: Stefan
authors.initials: S
authors.lastname: Dhein
mesh_terms: D000328:Adult; D000368:Aged; D000804:Angiotensin II / Q000502:physiology; D001281:Atrial Fibrillation / Q000503:physiopathology*; D016279:Atrial Function, Left / Q000502:physiology*; D016280:Atrial Function, Right / Q000502:physiology*; D005260:Female; D006325:Heart Atria / Q000378:metabolism*; D006349:Heart Valve Diseases / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008943:Mitral Valve; D011945:Receptors, Angiotensin / Q000096:biosynthesis*
chemical_list: D011945:Receptors, Angiotensin; D000804:Angiotensin II