title: In humans, chronic atrial fibrillation decreases the transient outward current and ultrarapid component of the delayed rectifier current differentially on each atria and increases the slow component of the delayed rectifier current in both.
abstract: OBJECTIVE
  The purpose of this study was to compare the voltage-dependent K(+) currents of human cells of the right and left atria and determine whether electrical remodeling produced by chronic atrial fibrillation (CAF) is chamber-specific.
  
  
  BACKGROUND
  Several data point to the existence of interatrial differences in the repolarizing currents. Therefore, it could be possible that CAF-induced electrical remodeling differentially affects voltage-dependent K(+) currents in each atrium.
  
  
  METHODS
  Currents were recorded using the whole-cell patch-clamp in myocytes from left (LAA) and right atrial appendages (RAA) obtained from sinus rhythm (SR) and CAF patients.
  
  
  RESULTS
  In SR, LAA and RAA myocytes were divided in 3 types, according to their main voltage-dependent repolarizing K(+) current. CAF differentially modified the proportion of these 3 types of cells on each atrium. CAF reduced the Ca(2+)-independent 4-aminopyridine-sensitive component of the transient outward current (I(to1)) more markedly in the LAA than in the RAA. Therefore, an atrial right-to-left I(to1) gradient was created by CAF. In contrast, the ultrarapid component of the delayed rectifier current (I(Kur)) was more markedly reduced in the RAA than in the LAA, thus abolishing the atrial right-to-left I(Kur) gradient observed in SR. Importantly, in both atria, CAF increased the slow component of the delayed rectifier current (I(Ks)).
  
  
  CONCLUSIONS
  Our results demonstrated that in SR there are intra-atrial heterogeneities in the repolarizing currents. CAF decreases I(to1) and I(Kur) differentially in each atrium and increases I(Ks) in both atria, an effect that further promotes re-entry.
authors.affiliation: Department of Pharmacology, School of Medicine, Universidad Complutense de Madrid, Madrid, Spain.
authors.forename: Ricardo
authors.initials: R
authors.lastname: Caballero
authors.forename: Marta González
authors.initials: MG
authors.lastname: de la Fuente
authors.forename: Ricardo
authors.initials: R
authors.lastname: Gómez
authors.forename: Adriana
authors.initials: A
authors.lastname: Barana
authors.forename: Irene
authors.initials: I
authors.lastname: Amorós
authors.forename: Pablo
authors.initials: P
authors.lastname: Dolz-Gaitón
authors.forename: Lourdes
authors.initials: L
authors.lastname: Osuna
authors.forename: Jesús
authors.initials: J
authors.lastname: Almendral
authors.forename: Felipe
authors.initials: F
authors.lastname: Atienza
authors.forename: Francisco
authors.initials: F
authors.lastname: Fernández-Avilés
authors.forename: Ana
authors.initials: A
authors.lastname: Pita
authors.forename: Jorge
authors.initials: J
authors.lastname: Rodríguez-Roda
authors.forename: Angel
authors.initials: A
authors.lastname: Pinto
authors.forename: Juan
authors.initials: J
authors.lastname: Tamargo
authors.forename: Eva
authors.initials: E
authors.lastname: Delpón
mesh_terms: D001281:Atrial Fibrillation / Q000175:diagnosis* / Q000188:drug therapy / Q000503:physiopathology; D002908:Chronic Disease; D004562:Electrocardiography; D004594:Electrophysiology; D005260:Female; D006325:Heart Atria / Q000166:cytology / Q000378:metabolism; D006801:Humans; D015640:Ion Channel Gating / Q000187:drug effects; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*; D012494:Sampling Studies
chemical_list: D026902:Potassium Channel Blockers; D015221:Potassium Channels