Diastolic stretch increases Ca2+ spark rate in atrial myocytes via a microtubule-dependent, ROS-independent mechanism, which could alter force generation or arrhythmogenesis.
n this issue of the Journal of the American Heart Association (JAHA), Fu et al 1 identified a new class of stretch-dependent Ca 2+ signaling events in atrial myocytes of rabbits, pigs, and humans.Such changes in Ca 2+ signaling could alter force generation or arrhythmogenesis in the affected cells.The team members who did this work were from the Universities of Freiburg, Maastricht, and Ghent, and they showed that diastolic stretch of freshly isolated left atrial cardiomyocytes provoked an increase in the Ca 2+ spark rate in the stretched region.This increase in the Ca 2+ spark rate was by a notably different mechanism than the increases in Ca 2+ spark rate reported by Prosser et al 2 in rodent ventricular myocytes because the increase in Ca 2+ spark rate did not depend on an elevation in local reactive oxygen species (ROS).However, intact microtubules were required for both types of stretch-induced Ca 2+ spark increase.Therefore, the term microtubuledependent Ca 2+ spark recruitment may more accurately describe these findings.
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Zhao et al. (2025) studied this question.
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