title: TASK-1 channels may modulate action potential duration of human atrial cardiomyocytes.
abstract: OBJECTIVE
  Atrial fibrillation is the most common arrhythmia in the elderly, and potassium channels with atrium-specific expression have been discussed as targets to treat atrial fibrillation. Our aim was to characterize TASK-1 channels in human heart and to functionally describe the role of the atrial whole cell current I(TASK-1).
  
  
  RESULTS
  Using quantitative PCR, we show that TASK-1 is predominantly expressed in the atria, auricles and atrio-ventricular node of the human heart. Single channel recordings show the functional expression of TASK-1 in right human auricles. In addition, we describe for the first time the whole cell current carried by TASK-1 channels (I(TASK-1)) in human atrial tissue. We show that I(TASK-1) contributes to the sustained outward current I(Ksus) and that I(TASK-1) is a major component of the background conductance in human atrial cardiomyocytes. Using patch clamp recordings and mathematical modeling of action potentials, we demonstrate that modulation of I(TASK-1) can alter human atrial action potential duration.
  
  
  CONCLUSIONS
  Due to the lack of ventricular expression and the ability to alter human atrial action potential duration, TASK-1 might be a drug target for the treatment of atrial fibrillation.
authors.affiliation: Institut für Physiologie und Pathophysiologie, Abteilung vegetative Physiologie, Universität Marburg, Deutschhausstraße 1-2, Marburg, Germany.
authors.forename: Sven H
authors.initials: SH
authors.lastname: Limberg
authors.forename: Michael F
authors.initials: MF
authors.lastname: Netter
authors.forename: Caroline
authors.initials: C
authors.lastname: Rolfes
authors.forename: Susanne
authors.initials: S
authors.lastname: Rinné
authors.forename: Günter
authors.initials: G
authors.lastname: Schlichthörl
authors.forename: Marylou
authors.initials: M
authors.lastname: Zuzarte
authors.forename: Timon
authors.initials: T
authors.lastname: Vassiliou
authors.forename: Rainer
authors.initials: R
authors.lastname: Moosdorf
authors.forename: Hinnerk
authors.initials: H
authors.lastname: Wulf
authors.forename: Jürgen
authors.initials: J
authors.lastname: Daut
authors.forename: Frank B
authors.initials: FB
authors.lastname: Sachse
authors.forename: Niels
authors.initials: N
authors.lastname: Decher
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000368:Aged; D000818:Animals; D001281:Atrial Fibrillation / Q000378:metabolism / Q000473:pathology; D002478:Cells, Cultured; D004562:Electrocardiography; D005260:Female; D006325:Heart Atria / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000502:physiology*; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism*; D009865:Oocytes / Q000378:metabolism; D018408:Patch-Clamp Techniques; D024683:Potassium Channels, Tandem Pore Domain / Q000235:genetics / Q000378:metabolism*; D014981:Xenopus
chemical_list: D009419:Nerve Tissue Proteins; D024683:Potassium Channels, Tandem Pore Domain; C420132:potassium channel subfamily K member 3