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Updated: Jun 10, 2026

Isolation of Atrial Myocytes from Adult Mice
08:34

Isolation of Atrial Myocytes from Adult Mice

Published on: July 25, 2019

Role of constitutively active acetylcholine-mediated potassium current in atrial contractile dysfunction caused by

Sang-Ho Koo1, Reza Wakili, Jung-Ho Heo

  • 1Division of Cardiology, Department of Internal Medicine, Kosin University School of Medicine, 34 Amnam-Dong, Seo-Ku, Busan 602-702, South Korea.

Europace : European Pacing, Arrhythmias, and Cardiac Electrophysiology : Journal of the Working Groups on Cardiac Pacing, Arrhythmias, and Cardiac Cellular Electrophysiology of the European Society of Cardiology
|August 5, 2010
PubMed

Insights

Increased acetylcholine-regulated potassium current (I(KAChc)) contributes to atrial fibrillation (AF)-related contractile dysfunction. Blocking this current may prevent AF-related thrombo-embolic complications.

Area of Science:

  • Cardiology
  • Electrophysiology
  • Molecular Cardiology

Background:

  • Atrial fibrillation (AF) poses a significant risk for thrombo-embolic stroke.
  • Atrial cardiomyocytes possess a constitutively active acetylcholine-regulated K(+)-current (I(KAChc)) that is upregulated during atrial tachycardia (AT).
  • I(KAChc) influences action potential duration (APD), thereby affecting cardiac contractility through calcium handling.

Purpose of the Study:

  • To investigate the role of I(KAChc) in AF-associated contractile dysfunction.
  • To determine if I(KAChc) up-regulation contributes to the reduced contractility observed in AT.
  • To explore I(KAChc) as a potential therapeutic target for AF complications.

Main Methods:

  • Canine models were used, divided into control and AT groups (400 bpm for 7 days).
  • Tertiapin-Q (TQ), a selective I(KAChc) blocker, was administered to assess its effects.
  • Measurements included single-cell left atrial (LA) intracellular Ca(2+)-transients (CaTrs), cell-shortening (CS), and whole LA tissue tension.

Main Results:

  • AT significantly increased I(KAChc) and decreased whole LA contractility compared to controls.
  • Administration of TQ partially reversed the AT-induced decrease in contractility and CaTr amplitude.
  • Single-cell measurements showed reduced CaTr amplitude and CS in AT, which were partly restored by TQ.

Conclusions:

  • Upregulated I(KAChc) plays a crucial role in AF-related contractile dysfunction.
  • Targeting I(KAChc) could be a novel strategy to prevent hypocontractility-related thrombo-embolic events in AF patients.
Abstract

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