Pulmonary vein sleeve cell excitation-contraction-coupling becomes dysynchronized by spontaneous calcium transients

Katja Rietdorf*, Said Masoud, Fraser McDonald, Michael J. Sanderson, Martin D. Bootman

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)

Abstract

Atrial fibrillation (AF) is the most common form of sustained cardiac arrhythmia. Substantial evidence indicates that cardiomyocytes located in the pulmonary veins [pulmonary vein sleeve cells (PVCs)] cause AF by generating ectopic electrical activity. Electrical ablation, isolating PVCs from their left atrial junctions, is a major treatment for AF. In small rodents, the sleeve of PVCs extends deep inside the lungs and is present in lung slices. Here we present data, using the lung slice preparation, characterizing how spontaneous Ca<sup>2+</sup> transients in PVCs affect their capability to respond to electrical pacing. Immediately after a spontaneous Ca<sup>2+</sup> transient the cell is in a refractory period and it cannot respond to electrical stimulation. Consequently, we observe that the higher the level of spontaneous activity in an individual PVC, the less likely it is that this PVC responds to electrical field stimulation. The spontaneous activity of neighbouring PVCs can be different from each other. Heterogeneity in the Ca<sup>2+</sup> signalling of cells and in their responsiveness to electrical stimuli are known pro-arrhythmic events. The tendency of PVCs to show spontaneous Ca<sup>2+</sup> transients and spontaneous action potentials (APs) underlies their potential to cause AF.

Original languageEnglish
Pages (from-to)410-416
Number of pages7
JournalBiochemical Society Transactions
Volume43
DOIs
Publication statusPublished - 1 Jun 2015

Keywords

  • Atrial fibrillation
  • Calcium signalling
  • Cardiac arrhythmia
  • Lung slice
  • Pulmonary vein myocyte

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