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Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
10:53

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Published on: July 3, 2013

Inhibition of ultra-rapid delayed rectifier K+ current by verapamil in human atrial myocytes

Zhan Gao1, Chu-Pak Lau, Shui-Wah Chiu

  • 1Department of Medicine, and Institute of Cardiovascular Science and Medicine, Faculty of Medicine, The University of Hong Kong, 21 Sassoon Road, Pokfulam, Hong Kong, China.

Journal of Molecular and Cellular Cardiology
|February 12, 2004
PubMed

Insights

Verapamil, a calcium channel blocker, inhibits the ultra-rapid delayed rectifier potassium current (I(Kur)) in human atrial cells. This drug does not affect the transient outward potassium current (I(to1)), potentially explaining its atrial effects.

Area of Science:

  • Cardiovascular pharmacology
  • Electrophysiology
  • Ion channel research

Background:

  • Verapamil is a common calcium channel antagonist for cardiovascular disorders.
  • Its effects on human atrial repolarization currents, specifically I(to1) and I(Kur), are not well understood.

Purpose of the Study:

  • To investigate the impact of verapamil on transient outward potassium current (I(to1)) and ultra-rapid delayed rectifier potassium current (I(Kur)) in human atrial myocytes.
  • To elucidate the mechanism of verapamil's action on these currents.

Main Methods:

  • Whole-cell patch-clamp electrophysiology was used to record ionic currents in isolated human atrial myocytes.
  • Verapamil's effects were assessed at varying concentrations (1-50 microM).

Main Results:

  • Verapamil did not inhibit I(to1) at concentrations up to 50 microM.
  • Verapamil demonstrated a reversible, concentration-dependent inhibition of I(Kur) with an IC(50) of 3.2 microM.
  • A concentration of 5 microM verapamil reduced I(Kur) by 61.3 +/- 7.5% and accelerated its inactivation, suggesting open channel block.

Conclusions:

  • Verapamil significantly blocks the I(Kur) repolarization current in human atrial cells.
  • Verapamil does not inhibit I(to1) in the human atrium.
  • The blockade of I(Kur) by verapamil may contribute to its therapeutic effects in atrial arrhythmias.

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