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Updated: Dec 30, 2025

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Antiarrhythmic effect of crotonoside by regulating sodium and calcium channels in rabbit ventricular myocytes
Zhipei Liu1, Yuzhong Jia2, Lv Song2
1Cardio-Electrophysiological Research Laboratory, Medical College of Wuhan University of Science and Technology, Wuhan 430065, China; Hubei Province Key Laboratory of Occupational Hazard Identification and Control, Medical College of Wuhan University of Science and Technology, Wuhan 430065, China.
Aims:
Detect the antiarrhythmic effect of crotonoside (Cro).
Main Methods:
We used whole-cell patch-clamp techniques to detect the effects of Cro on action potentials (APs) and transmembrane ion currents in isolated rabbit left ventricular myocytes. We also verified the effect of Cro on ventricular arrhythmias caused by aconitine in vivo.
Key Findings:
Cro reduced the maximum depolarization velocity (Vmax) of APs and shortened the action potential duration (APD) in a concentration-dependent manner, but it had no significant effect on the resting membrane potential (RMP) or action potential amplitude (APA). It also inhibited the peak sodium current (INa) and L-type calcium current (ICaL) in a concentration-dependent manner with half-maximal inhibitory concentrations (IC50) of 192 μmol/L and 159 μmol/L, respectively. However, Cro had no significant effects on the inward rectifier potassium current (IK1) or rapidly activating delayed rectifier potassium current (IKr). Sea anemone toxin II (ATX II) increased the late sodium current (INaL), but Cro abolished this effect. Moreover, Cro significantly abolished ATX II-induced early afterdepolarizations (EADs) and high extracellular Ca2+ concentration (3.6 mmol/L)-induced delayed afterdepolarizations (DADs). We also verified that Cro effectively delayed the onset time and reduced the incidence of ventricular arrhythmias caused by aconitine in vivo.
Significance:
These results revealed that Cro effectively inhibits INa, INaL, and ICaL in ventricular myocytes. Cro has antiarrhythmic potential and thus deserves further study.
Insights
Crotonoside (Cro) demonstrates antiarrhythmic effects by inhibiting key ion currents in heart cells. This compound effectively reduces ventricular arrhythmias in vivo, suggesting therapeutic potential.
Area of Science:
- Cardiovascular Pharmacology
- Electrophysiology
- Pharmacology
Background:
- Cardiac arrhythmias pose a significant health risk.
- Identifying novel antiarrhythmic agents is crucial for clinical management.
Purpose of the Study:
- To investigate the antiarrhythmic effects of crotonoside (Cro).
- To elucidate the mechanisms underlying Cro's action on cardiac ion channels and action potentials.
Main Methods:
- Whole-cell patch-clamp techniques were employed on isolated rabbit ventricular myocytes.
- Effects of Cro on action potentials and transmembrane ion currents were assessed.
- In vivo studies evaluated the efficacy of Cro against aconitine-induced ventricular arrhythmias.
Main Results:
- Crotonoside concentration-dependently reduced action potential upstroke velocity (Vmax) and action potential duration (APD).
- Cro inhibited peak sodium current (INa) and L-type calcium current (ICAL) with IC50 values of 192 μmol/L and 159 μmol/L, respectively.
- Cro abolished late sodium current (INaL) and suppressed both early and delayed afterdepolarizations, significantly reducing in vivo ventricular arrhythmias.
Conclusions:
- Crotonoside effectively inhibits INa, INaL, and ICAL in ventricular myocytes.
- Crotonoside exhibits significant antiarrhythmic potential, warranting further investigation for therapeutic applications.
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