Related Experiment Video
Updated: Jul 5, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Effect of alpha-allocryptopine on transient outward potassium current in rabbit ventricular myocytes
1Electrophysiology of Laboratory, Institute of Geriatric Cardiology, Chinese PLA General Hospital, Beijing, China.
Insights
Alpha-allocryptopine inhibits the transient outward potassium current (I(to)) in rabbit heart cells. This blocking effect on I(to) may explain its antiarrhythmic properties.
Area of Science:
- Cardiology
- Pharmacology
- Electrophysiology
Background:
- The transient outward potassium current (I(to)) plays a crucial role in cardiac repolarization.
- Understanding the modulators of I(to) is essential for developing antiarrhythmic therapies.
Purpose of the Study:
- To elucidate the mechanism by which alpha-allocryptopine inhibits I(to) in rabbit left-ventricular myocytes.
- To investigate the concentration-dependent and use-independent effects of alpha-allocryptopine on I(to).
Main Methods:
- Isolated rabbit left-ventricular myocytes were used.
- The whole-cell patch-clamp technique was employed to record I(to).
- Alpha-allocryptopine was applied at concentrations ranging from 1 to 100 microM.
Main Results:
- Alpha-allocryptopine significantly decreased I(to) amplitude and density in a concentration-dependent manner (IC(50) = 37 +/- 8 microM).
- The drug reduced I(to) inactivation time constants and altered the inactivation curve slope without affecting activation parameters.
- Allocryptopine decreased transmural heterogeneity and dispersion of I(to) in the ventricular myocytes.
Conclusions:
- Alpha-allocryptopine exhibits a direct blocking effect on I(to) in cardiac myocytes.
- This inhibition of I(to) is a potential mechanism underlying the antiarrhythmic effects of alpha-allocryptopine.
Objective:
To investigate the mechanism of alpha-allocryptopine-induced inhibition of the transient outward potassium current (I(to)) in rabbit left-ventricular myocytes.
Methods:
We used the whole-cell patch-clamp technique to record the I(to) in the myocytes, which were isolated from the rabbit left ventricle by a Langendorff-perfusion device.
Results:
Allocryptopine decreased the amplitude and the density of the I(to) in a concentration-dependent (range from 1 to 100 microM with an IC(50) value of 37 +/- 8 microM) and frequency- or use-independent manner. At a test potential of +50 mV, the peak current density of I(to) was decreased from 21.56 +/- 3.24 to 13.37 +/- 2.86 pA/pF by 30 microM allocryptopine. The fast time constant of I(to) inactivation was reduced from 9.8 +/- 1.8 to 5.7 +/- 0.7 ms and the slow time constant of I(to) was reduced from 50.8 +/- 9.0 to 32.2 +/- 12.7 ms by 30 microM allocryptopine. The inactivated curve slope was changed from -19.2 +/- 7.1 to -7.5 +/- 0.6 mV, while the half-activated voltage and activated curve slope and half-inactivated voltage values were not affected by allocryptopine. Transmural heterogeneity of the I(to) was decreased in the presence of allocryptopine. At a test potential of +50 mV, the densities of I(to) were reduced by 28.6% (epimyocardium), 50.3% (mid-myocardium) and 20.1% (endocardium) after exposure to 30 microM allocryptopine.Transmural dispersion of the I(to) was reduced from 11.2 +/- 1.2 to 4.7 +/- 0.6 pA/pF by 30 microM allocryptopine.
Conclusion:
Allocryptopine produced a blocking effect on the I(to) in cardiac myocytes, which may be an important mechanism in its antiarrhythmic effect.
Related Concept Videos
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers
Depolarizing Blockers: Mechanism of Action
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because succinylcholine...
G-Protein Gated Ion Channels
Sensory organs,...

