Key result
Homocysteine exposure significantly decreased transient outward potassium currents by 24.8% at 50 micromol/L and 38.4% at 500 micromol/L in human atrial myocytes.
Why the study?
Does homocysteine alter potassium currents in human atrial myocytes?
Does homocysteine alter potassium currents in human atrial myocytes?
Homocysteine causes electrophysiological disturbances in potassium currents in human atrial myocytes, providing a potential mechanism for its association with atrial fibrillation.
Answers are grounded in this paper and cite their sources.
May link homocysteine to AF risk via myocyte electrophysiology; hypothesis-generating and requires in vivo validation.
A large body of evidence indicates that elevated homocysteine (Hcy) levels portend an increased risk for atrial fibrillation. However, little is known about the electrophysiological effects of Hcy on atrial myocytes. The present study was conducted to investigate the direct effects of Hcy on ion channels in human atria. 2. Whole-cell patch-clamp techniques were used to record potassium currents in human atrial cells. 3. In human atrial myocytes, transient outward potassium currents were significantly decreased by 24.8 +/- 5.9 and 38.4 +/- 10.4% in the presence of 50 and 500 micromol/L Hcy, respectively. The ultrarapid delayed rectifier potassium currents were decreased by approximately 30% when exposed to 500 micromol/L Hcy. The inward rectifier potassium currents were increased by approximately 40% in the presence of 500 micromol/L Hcy. 4. The results of the present study indicate that Hcy, an important risk factor for atrial fibrillation, could cause electrophysiological disturbances of potassium currents in human atrial myocytes.
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Cai et al. (2007) studied this question. Homocysteine was evaluated on Potassium currents in human atrial cells. Homocysteine exposure significantly decreased transient outward potassium currents by 24.8% at 50 micromol/L and 38.4% at 500 micromol/L in human atrial myocytes.
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