Abstract
This study presents an analysis of the electrophysiological effects of aconitine, a toxic diterpenoid alkaloid derived from Aconitum plants, on neonatal rat ventricular myocytes (NRVMs). The research investigates the potential impact of aconitine on various ion currents and cardiac action potentials, shedding light on its arrhythmogenic properties. Whole-cell patch-clamp experiments were conducted to assess the effects of aconitine on delayed-rectifier K+ currents (IK(DR)) and inwardly rectifying K+ currents (IK(IR) in NRVMs. The findings indicate that aconitine exposure led to the inhibition of (IK(DR)) and (IK(IR)), suggesting its potential influence on cardiac repolarization and excitability. Notably, aconitine induced transient inward current (ITI) and early after-depolarizations (EADs) in a concentration- dependent manner, both of which have implications for cardiac arrhythmias. Moreover, the study examined the electrocardiogram changes in Sprague-Dawley rats upon aconitine injection, revealing a prolonged QT interval and the emergence of polymorphic ventricular tachycardia (VTs), indicative of arrhythmic effects. The study emphasizes the importance of understanding the electrophysiological impact of aconitine and similar compounds, considering their potential therapeutic applications and associated toxicities.
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