https://www.selleckchem.com/pr....oducts/autophinib.ht
g., in normal ventricular myocytes), besides the requirement of increasing inward currents and reducing outward currents as for phase-2 EADs, the occurrence of phase-3 EADs and TAs requires a substantially large increase of the L-type Ca2+ current and the slow component of the delayed rectifier K+ current. The presence of ICa,T (e.g., in neonatal and failing ventricular myocytes) can greatly reduce the thresholds of these two currents for phase-3 EADs and TAs. This implies that ICa,T may play an important role in arrhythmogenesis in
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