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Related Experiment Videos

Calcium waves driven by "sensitization" wave-fronts.

Markus Keller1, Joseph P Y Kao, Marcel Egger

  • 1Department of Physiology, University of Bern, Bühlplatz 5, CH-3012 Bern, Switzerland.

Cardiovascular Research
|March 6, 2007
PubMed
Summary
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Cellular calcium (Ca2+) waves are driven by sarcoplasmic reticulum (SR) overload and ryanodine receptor (RyR) sensitization, not Ca2+-induced Ca2+ release (CICR). This finding is crucial for understanding cardiac arrhythmias.

Area of Science:

  • Cardiology
  • Cellular Physiology
  • Biophysics

Background:

  • Cellular Ca(2+) waves are typically modeled as reaction-diffusion systems.
  • Ca(2+)-induced Ca(2+) release (CICR) from Ca(2+) stores is the established mechanism sustaining these waves.
  • Recent findings show ryanodine receptors (RyRs) on the sarcoplasmic reticulum (SR) are sensitized by luminal SR Ca(2+).

Purpose of the Study:

  • To investigate the role of RyR sensitization in driving cellular Ca(2+) waves.
  • To determine if SR overloading via SERCA, coupled with RyR sensitization, contributes to wave propagation.
  • To differentiate the contributions of RyR sensitization versus CICR in cardiac Ca(2+) wave dynamics.

Main Methods:

  • Utilized confocal imaging of the Ca(2+) indicator fluo-3.

Related Experiment Videos

  • Employed UV-flash photolysis of caged compounds to manipulate intracellular conditions.
  • Applied the whole-cell patch clamp technique in isolated guinea pig ventricular cardiomyocytes.

    • Main Results:

    • Slowing of the SR Ca(2+)-ATPase (SERCA) with a photoreleased inhibitor immediately decelerated Ca(2+) waves.
    • No immediate secondary changes in Ca(2+) signaling or SR Ca(2+) content were observed.
    • Results support a model where SR loading and RyR sensitization propagate waves.

    Conclusions:

    • Ca(2+) loading leads to a propagating zone of RyR sensitization within the SR.
    • CICR is not the predominant mechanism driving cardiac Ca(2+) waves.
    • Understanding RyR sensitization is vital for conceptualizing arrhythmias from spontaneous Ca(2+) release.