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Updated: Jul 13, 2026

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

Homocysteine inhibits potassium channels in human atrial myocytes

Ben-Zhi Cai1, Dong-Mei Gong, Yu Liu

  • 1Department of Pharmacology, Harbin Medical University, Harbin, China.

Clinical and Experimental Pharmacology & Physiology
|July 25, 2007
PubMed

Insights

Elevated homocysteine (Hcy) impacts heart rhythm. This study shows Hcy disrupts potassium currents in human atrial cells, potentially explaining its link to atrial fibrillation.

Area of Science:

  • Cardiology
  • Electrophysiology
  • Molecular Biology

Background:

  • Elevated homocysteine (Hcy) levels are linked to increased risk of atrial fibrillation.
  • The direct electrophysiological effects of Hcy on atrial myocytes remain largely unknown.

Purpose of the Study:

  • To investigate the direct effects of homocysteine on ion channels in human atrial myocytes.
  • To understand the electrophysiological disturbances caused by Hcy in the human atria.

Main Methods:

  • Whole-cell patch-clamp techniques were utilized.
  • Potassium currents in human atrial cells were recorded and analyzed.

Main Results:

  • Homocysteine significantly decreased transient outward potassium currents.
  • Ultrarapid delayed rectifier potassium currents were reduced by Hcy.
  • Inward rectifier potassium currents were increased in the presence of Hcy.

Conclusions:

  • Homocysteine causes significant electrophysiological disturbances in human atrial myocytes.
  • These disturbances involve alterations in key potassium currents.
  • Hcy's effects on ion channels may underlie its association with atrial fibrillation.

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