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. Author manuscript; available in PMC: 2017 Jan 11.
Published in final edited form as: Prog Biophys Mol Biol. 2016 Jan 11;120(1-3):199–209. doi: 10.1016/j.pbiomolbio.2015.12.015

Figure 2.

Figure 2

Myocyte electrophysiological responses to sympathetic stimulation. NE binding to β-ARs activates PKA, which phosphorylates several intracellular targets, including IKs, ICaL, RyR, and PLB. Phosphorylation of IKs leads to APD shortening that may increase the dispersion of repolarization due to non-uniform innervation and resulting spatially non-uniform β-AR activation. Phosphorylation of ICaL, RyR, and PLB lead to increased intracellular [Ca2+], increased SR Ca2+ leak, and increased SR Ca2+ load. Collectively, these conditions are favorable for EAD and DAD formation. EADs may contribute to increased dispersion of repolarization and both EADs and DADs contribute to ectopic activity and focal arrhythmia.