title: Spironolactone prevents aldosterone induced increased duration of atrial fibrillation in rat.
abstract: BACKGROUND
  Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice. The Renin-Angiotensin-Aldosterone-System plays a major role for the atrial structural and electrical remodelling. Recently elevated aldosterone levels have been suggested to increase the risk for the development of AF.
  
  
  METHODS
  Rats were treated with aldosterone by means of an osmotic minipump (0.5μg/h) over a period of 4 weeks. AF was induced by transesophageal burst pacing. Action potentials (AP) were recorded from left atrial preparations with microelectrodes. Atrial collagen was quantified by histological studies.
  
  
  RESULTS
  Aldosterone treatment resulted in hypertrophy as indicated by an increased ratio of heart weight/tibia length and doubled the time until the AF converted spontaneously into sinus rhythm (85.8±13.4 s vs. 38.3±6.9 s, p<0.01). This was associated with a significant shortening of the AP (APD90 26.2±1.1 vs. 31.2±1.9, p<0.05) and an increased protein expression of Kir2.1 and Kv1.5. Atrial collagen deposition was significantly greater in aldosterone-treated rats. The alterations could be prevented by additional application spironolactone.
  
  
  CONCLUSIONS
  The results of the present study suggest that in addition to the structural remodelling aldosterone also promotes AF by altering repolarising potassium currents leading to action potential shortening.
authors.affiliation: Department of Internal Medicine III, University of Cologne, Cologne, Germany.
authors.forename: Carina
authors.initials: C
authors.lastname: Lammers
authors.forename: Theresa
authors.initials: T
authors.lastname: Dartsch
authors.forename: Mathias C
authors.initials: MC
authors.lastname: Brandt
authors.forename: Dennis
authors.initials: D
authors.lastname: Rottländer
authors.forename: Marcel
authors.initials: M
authors.lastname: Halbach
authors.forename: Gabriel
authors.initials: G
authors.lastname: Peinkofer
authors.forename: Simon
authors.initials: S
authors.lastname: Ockenpoehler
authors.forename: Marco
authors.initials: M
authors.lastname: Weiergraeber
authors.forename: Toni
authors.initials: T
authors.lastname: Schneider
authors.forename: Hannes
authors.initials: H
authors.lastname: Reuter
authors.forename: Jochen
authors.initials: J
authors.lastname: Müller-Ehmsen
authors.forename: Jürgen
authors.initials: J
authors.lastname: Hescheler
authors.forename: Uta C
authors.initials: UC
authors.lastname: Hoppe
authors.forename: Carsten
authors.initials: C
authors.lastname: Zobel
mesh_terms: D000200:Action Potentials; D000450:Aldosterone / Q000009:adverse effects* / Q000494:pharmacology; D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology / Q000517:prevention & control*; D001794:Blood Pressure; D015153:Blotting, Western; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013148:Spironolactone / Q000494:pharmacology*
chemical_list: D013148:Spironolactone; D000450:Aldosterone