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. 2015 Apr 29;6:9. doi: 10.1186/s13293-015-0027-9

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© Ayaz and Howlett; licensee BioMed Central. 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Impact of GDX on intracellular Ca²⁺-handling mechanisms in ventricular myocytes isolated from rodent hearts. APD is prolonged by GDX, due to a decrease in repolarizing K⁺ currents (I_Kur) and a reduction in the expression of Kv1.5. Reduced Ca²⁺ influx along with smaller Ca²⁺ sparks attenuates SR Ca²⁺ release. Ca²⁺ transient decay is slowed by longer APs and slower SR Ca²⁺ uptake mediated by a decrease in phosphorylation of PLB by CaMKII (and possibly PKA). Peak contractions are attenuated through smaller peak Ca²⁺ transients and a decrease in maximal myofilament responsiveness to Ca²⁺. Contractions are slowed because SR Ca²⁺ uptake is reduced and the slower β-MHC isoform predominates. Whether NCX activity or expression is affected by GDX is not yet clear.