Isoliensinine Eliminates Afterdepolarizations Through Inhibiting Late Sodium Current and L-Type Calcium Current

Isoliensinine (IL) extracted from lotus seed has a good therapeutic effect on cardiovascular diseases. However, its effect on ion channels of ventricular myocytes is still unclear. We used whole-cell patch-clamp techniques to detect the effects of IL on transmembrane ion currents and action potential (AP) in isolated rabbit left ventricular myocytes. IL inhibited the transient sodium current ( I NaT ), late sodium current ( I NaL ) enlarged by sea anemone toxin (ATX II) and L-type calcium current ( I CaL ) in a concentration-dependent manner without affecting inward rectifier potassium current ( I K1 ) and delayed rectifier potassium current ( I K ). These inhibitory effects are mainly manifested as reduced the AP amplitude (APA) and maximum depolarization velocity ( V max ) and shortened the action potential duration (APD), but had no significant effect on the resting membrane potential (RMP). Moreover, IL significantly eliminated ATX II-induced early afterdepolarizations (EADs) and high extracellular calcium-induced delayed afterdepolarizations (DADs). These results revealed that IL effectively eliminated EADs and DADs through inhibiting I NaL and I CaL in ventricular myocytes, which indicates it has potential antiarrhythmic action.