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

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Published on: July 3, 2013

Proarrhythmic effect of blocking the small conductance calcium activated potassium channel in isolated canine left

Chia-Hsiang Hsueh1, Po-Cheng Chang, Yu-Cheng Hsieh

  • 1Krannert Institute of Cardiology and Division of Cardiology, Indiana University, Indianapolis, Indiana 46202, USA.

Heart Rhythm
|February 5, 2013
PubMed
Abstract

Insights

Blocking small conductance calcium-activated potassium (SKCa) channels in the canine left atrium prolonged action potential duration and increased arrhythmia incidence. This suggests SKCa channels play a role in regulating atrial electrical stability.

Area of Science:

  • Cardiovascular Physiology
  • Electrophysiology
  • Ion Channel Function

Background:

  • Small conductance calcium-activated potassium (SKCa) channels are intracellular calcium-activated and voltage-insensitive.
  • Genetic studies link SKCa channel variants to lone atrial fibrillation in humans.
  • The precise role of SKCa channels in atrial arrhythmias remains largely unknown.

Purpose of the Study:

  • To investigate the functional role of SKCa channels in the development of atrial arrhythmias.
  • To determine how SKCa channel blockade affects atrial action potential duration and electrical stability.

Main Methods:

  • Utilized optical mapping techniques on isolated canine left atria.
  • Evaluated changes in action potential duration (APD) and arrhythmia induction before and after administration of SKCa channel blockers (apamin or UCL-1684).

Main Results:

  • SKCa channel blockade significantly increased action potential duration (APD₈₀) and APD heterogeneity.
  • The thresholds for inducing 2:2 alternans and wave breaks were prolonged by SKCa channel blockade.
  • Following SKCa channel blockade, 4 out of 6 atria developed arrhythmias, whereas none did at baseline.

Conclusions:

  • SKCa channel blockade promotes atrial arrhythmia in the canine model.
  • Increased APD heterogeneity is a likely mechanism for the proarrhythmic effects of SKCa channel blockade.
  • Findings support genetic associations between KCNN3 (encoding SKCa channels) and lone atrial fibrillation.

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