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XB-ART-45161
Cell Physiol Biochem 2011 Jan 01;284:613-24. doi: 10.1159/000335757.
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TASK-1 channels may modulate action potential duration of human atrial cardiomyocytes.

Limberg SH, Netter MF, Rolfes C, Rinné S, Schlichthörl G, Zuzarte M, Vassiliou T, Moosdorf R, Wulf H, Daut J, Sachse FB, Decher N.


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BACKGROUND/AIMS: 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). METHODS AND 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. CONCLUSION: 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.

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Species referenced: Xenopus
Genes referenced: kcnk3

References [+] :
Abbruzzese, Modification of hERG1 channel gating by Cd2+. 2010, Pubmed, Xenbase