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Updated: Apr 12, 2026

Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique
Published on: November 11, 2022
THE INHIBITORY EFFECT OF PACLITAXEL ON (Kv2.1) K+ CURRENT IN H9c2 CELLS
Naoko Kitamura1, Kazuho Sakamoto, Tomoyuki Ono
1Department of Pharmacology, Fukushima Medical University, School of Medicine.
Abstract:
Using the whole-cell voltage clamp technique, we investigated the effect of paclitaxel, an anticancer agent which promotes microtubule formation, on K(+) current in H9c2 cells originated from rat embryonic cardiac myocytes. Paclitaxel inhibited Kv2.1 voltage-dependent K(+) current (IKur) with ultra-rapidly activating and slowly inactivating kinetics in a concentration-dependent manner. The inhibitory effect of paclitaxel on IKur was time-dependent and more marked at 200 ms after the onset than at the beginning of the depolarizing pulse. The IC50 value of paclitaxel was 1.1 µM at 200 ms. The time-dependent inhibition suggests that paclitaxel might be an open channel blocker of Kv2.1. This inhibition of Kv2.1 may be involved in the adverse effects of paclitaxel on cardiac and neuronal cells.
Insights
Paclitaxel, an anticancer drug, inhibits a key potassium channel (Kv2.1) in heart cells. This action may explain some of paclitaxel
Area of Science:
- Cardiovascular Pharmacology
- Ion Channel Physiology
- Cancer Therapeutics
Background:
- Paclitaxel is a widely used chemotherapy agent.
- Cardiac and neuronal side effects are associated with paclitaxel treatment.
- Kv2.1 channels play a crucial role in cardiac myocyte electrophysiology.
Purpose of the Study:
- To investigate the effect of paclitaxel on K(+) current in H9c2 cells.
- To determine the specific potassium channel subtype affected by paclitaxel.
- To elucidate the mechanism of paclitaxel's interaction with Kv2.1 channels.
Main Methods:
- Whole-cell voltage clamp technique.
- H9c2 cell line derived from rat embryonic cardiac myocytes.
- Concentration- and time-dependent analysis of ion channel currents.
Main Results:
- Paclitaxel inhibited the Kv2.1 voltage-dependent K(+) current (IKur).
- Inhibition was concentration-dependent with an IC50 of 1.1 µM at 200 ms.
- The time-dependent inhibition suggests paclitaxel acts as an open channel blocker.
Conclusions:
- Paclitaxel inhibits Kv2.1 potassium channels in cardiac myocytes.
- This inhibition may contribute to the cardiotoxicity of paclitaxel.
- Understanding this mechanism could inform strategies to mitigate paclitaxel's adverse effects.
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