https://www.selleckchem.com/products/secinh3.html
Ventricular myocytes and tubulated atrial myocytes additionally exhibited early afterdepolarizations (EADs) during hypokalemia, associated with Ca2+ overload. However, EADs also occurred in untubulated atrial cells, despite Ca2+ quiescence. These phase-3 EADs were rather linked to reactivation of non-equilibrium Na+ current, as they were rapidly blocked by tetrodotoxin. Na+ current-driven EADs in untubulated atrial cells were enabled by membrane hyperpolarization during hypokalemia and short action potential configurations. Brief action
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