Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8473754 | Journal of Molecular and Cellular Cardiology | 2016 | 27 Pages |
Abstract
Activation of ICl(Ca) in canine ventricular cells requires Ca2+-entry through neighboring L-type Ca2+ channels and is only augmented by SR Ca2+-release. Substantial activation of ICl(Ca) requires high Ca2+ concentration in the dyadic clefts which can be effectively buffered by BAPTA, but not EGTA.
Keywords
9-anthracene carboxylic acidICl(Ca)Ca2+-dependent inactivationSITSLarge-conductance Ca2+-activated K+ channelsIncXTMEM16A9-ACCaV1.2LTCCAPD90[Cl−]iDIDSRyRHEPESPCCCDICATIKSDAPIDAD4′,6-diamidino-2-phenylindole4-(2-Hydroxyethyl)piperazine-1-ethanesulfonic acidBKCaICa,LL-type Ca2+ current[Ca2+]iISOisoproterenolstandard error of the meanSarcoplasmic reticulumPearson correlation coefficientintracellular Cl− concentrationSEMaction potentialdelayed afterdepolarizationHuman cardiomyocytesL-type Ca2+ channelCICRCalcium transientRyanodine receptor
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Authors
Balázs Horváth, Krisztina Váczi, Bence Hegyi, Mónika Gönczi, Beatrix Dienes, Kornél Kistamás, Tamás Bányász, János Magyar, István Baczkó, András Varró, György Seprényi, László Csernoch, Péter P. Nánási, Norbert Szentandrássy,