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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