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Related Experiment Videos

Intracellular Ca2+ release contributes to automaticity in cat atrial pacemaker cells.

J Hüser1, L A Blatter, S L Lipsius

  • 1Department of Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153, USA.

The Journal of Physiology
|April 15, 2000
PubMed
Summary

Low voltage-activated calcium current (ICa,T) triggers calcium sparks in atrial pacemaker cells. This sparks stimulate sodium-calcium exchange, driving heart rhythm and potentially causing arrhythmias.

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Area of Science:

  • Cardiology
  • Cellular Electrophysiology
  • Calcium Signaling

Background:

  • Cardiac atrial pacemaker activity regulation remains incompletely understood.
  • Intracellular calcium release's role in pacemaker automaticity requires further elucidation.

Purpose of the Study:

  • To investigate the contribution of intracellular Ca2+ release to the automaticity of cat right atrial pacemaker cells.
  • To clarify the cellular mechanisms governing cardiac atrial pacemaker activity.

Main Methods:

  • Perforated patch voltage clamp recordings.
  • Confocal fluorescence microscopy.
  • Isolation of pacemaker cells from cat right atrium.

Main Results:

  • Subsarcolemmal intracellular Ca2+ release (Ca2+ sparks) occurred during late diastolic depolarization.

Related Experiment Videos

  • Blockade of low voltage-activated T-type Ca2+ current (ICa,T) with Nickel (Ni2+) suppressed Ca2+ sparks and slowed pacemaker rate.
  • Low voltage-activated Ca2+ release, triggered around -60 mV, was paralleled by Na+-Ca2+ exchange current (INa-Ca) and observed in sino-atrial and latent atrial pacemaker cells.

    • Conclusions:

    • Low voltage-activated ICa,T initiates subsarcolemmal Ca2+ sparks, which then activate INa-Ca, leading to pacemaker potential depolarization.
    • This mechanism highlights the critical roles of ICa,T and subsarcolemmal Ca2+ release in normal atrial pacing.
    • The findings may offer insights into the development of ectopic atrial arrhythmias.