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Triggered activity in atrial myocytes is influenced by Na+/Ca2+ exchanger activity in genetically altered mice

In atrial fibrillation, increased function of the Na+/Ca2+-exchanger (NCX) is one among several electrical remodeling mechanisms. Using the patch-clamp- and Ca2+ imaging-methods, we investigated atrial myocytes from NCX-homozygous-overexpressor (OE)- and heterozygous-knockout (KO)-mice and their cor...

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Published in:Journal of molecular and cellular cardiology 2016-12, Vol.101, p.106-115
Main Authors: Bögeholz, N., Pauls, P., Kaese, S., Schulte, J.S., Lemoine, M.D., Dechering, D.G., Frommeyer, G., Goldhaber, J.I., Seidl, M.D., Kirchhefer, U., Eckardt, L., Müller, F.U., Pott, C.
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Language:English
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Summary:In atrial fibrillation, increased function of the Na+/Ca2+-exchanger (NCX) is one among several electrical remodeling mechanisms. Using the patch-clamp- and Ca2+ imaging-methods, we investigated atrial myocytes from NCX-homozygous-overexpressor (OE)- and heterozygous-knockout (KO)-mice and their corresponding wildtypes (WTOE; WTKO). NCX mediated Ca2+ extrusion capacity was reduced in KO and increased in OE. There was no evidence for structural or molecular remodeling. During a proarrhythmic pacing-protocol, the number of low amplitude delayed afterdepolarizations (DADs) was unaltered in OE vs. WTOE and KO vs. WTKO. However, DADs triggered full spontaneous action potentials (sAP) significantly more often in OE vs. WTOE (ratio sAP/DAD: OE:0.18±0.05; WTOE:0.02±0.02; p
ISSN:0022-2828
1095-8584
DOI:10.1016/j.yjmcc.2016.11.004