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Shaping a New Ca2+ Conductance to Suppress Early Afterdepolarizations in Cardiac Myocytes
Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine at University of California, LosAngeles, CA 90095-7115, USA.
Department of Medicine (Cardiology), Cardiovascular Research Laboratory, David Geffen School of Medicine at University of California, LosAngeles, CA 90095-7115, USA.
Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine at University of California, Los Angeles, CA 90095-7115, USA.
Department of Medicine (Cardiology), Departments of Integrative Biology and Physiology, David Geffen School of Medicine at University of California, Los Angeles, CA 90095-7115, USA.
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2011 (Engelska)Ingår i: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 589, nr 24, s. 6081-6092Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Non‐technical summary Diseases, genetic defects, or ionic imbalances can alter the normal electrical activity of cardiac myocytes causing an anomalous heart rhythm, which can degenerate to ventricular fibrillation (VF) and sudden cardiac death. Well‐recognized triggers for VF are aberrations of the cardiac action potential, known as early afterdepolarizations (EADs). In this study, combining mathematical modelling and experimental electrophysiology in real‐time (dynamic clamp), we investigated the dependence of EADs on the biophysical properties of the L‐type Ca2+ current (ICa,L) and identified modifications of ICa,L properties which effectively suppress EAD. We found that minimal changes in the voltage dependence of activation or inactivation of ICa,L can dramatically reduce the occurrence of EADs in cardiac myocytes exposed to different EAD‐inducing conditions. This work assigns a critical role to the L‐type Ca2+ channel biophysical properties for EADs formation and identifies the L‐type Ca2+ channel as a promising therapeutic target to suppress EADs and their arrhythmogenic effects.

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John Wiley & Sons, 2011. Vol. 589, nr 24, s. 6081-6092
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Biofysik
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URN: urn:nbn:se:liu:diva-162177DOI: 10.1113/jphysiol.2011.219600OAI: oai:DiVA.org:liu-162177DiVA, id: diva2:1371958
Tillgänglig från: 2019-11-21 Skapad: 2019-11-21 Senast uppdaterad: 2019-11-26Bibliografiskt granskad

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Pantazis, Antonios

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