Why the study?
Does the knock-out of the TASK-1 potassium channel alter cardiac electrophysiology and conduction in mice?
Does the knock-out of the TASK-1 potassium channel alter cardiac electrophysiology and conduction in mice?
TASK-1 plays a regulatory role in the cardiac conduction system, as its knock-out in mice leads to prolonged QTc and broadened QRS intervals.
No immediate clinical implications; leaves open TASK-1's translational role in human conduction and anesthesia responses.
BACKGROUND/AIMS: The aim of the study was to characterize the whole cell current of the two-pore domain potassium channel TASK-1 (K2P3) in mouse ventricular cardiomyocytes (I(TASK-1)) and to analyze the cardiac phenotype of the TASK-1(-/-) mice. METHODS AND RESULTS: We have quantified the ventricular I(TASK-1) current using the blocker A293 and TASK-1(-/-) mice. Surface electrocardiogram recordings of TASK-1(-/-) mice showed a prolonged QTc interval and a broadened QRS complex. The differences in electrocardiograms between wild type and TASK-1(-/-) mice disappeared during sympathetic stimulation of the animals. Quantitative RT-PCR, patch clamp recordings and measurements of hemodynamic performance of TASK-1(-/-) mice revealed no major compensatory changes in ion channel transcription. Action potential recordings of TASK-1(-/-) mouse cardiomyocytes indicated that I(TASK-1) modulates action potential duration. Our in vivo electrophysiological studies showed that isoflurane, which activates TASK-1, slowed heart rate and atrioventricular conduction of wild-type but not of TASK-1(-/-) mice. CONCLUSION: The results of an invasive electrophysiological catheter protocol in combination with the observed QRS time prolongation in the surface electrocardiogram point towards a regulatory role of TASK-1 in the cardiac conduction system.
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Decher et al. (2011) studied this question.
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