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Related Experiment Videos

Activators of protein kinase C decrease Ca2+ spark frequency in smooth muscle cells from cerebral arteries

A D Bonev1, J H Jaggar, M Rubart

  • 1Department of Pharmacology, College of Medicine, University of Vermont, Colchester 05446, USA.

The American Journal of Physiology
|January 22, 1998
PubMed
Summary
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Ca(2+)-activated potassium channels and ATP-sensitive potassium channels as modulators of vascular tone.

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Protein kinase C (PKC) activators reduce calcium sparks and spontaneous transient outward currents (STOCs) in arterial myocytes. This modulation of calcium sparks by PKC influences KCa channel activity and membrane potential, impacting vasodilation.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cell Biology
  • Ion Channel Function

Background:

  • Local calcium (Ca2+) release from the sarcoplasmic reticulum (SR) via ryanodine receptors (RyRs) forms Ca2+ sparks.
  • Ca2+ sparks activate Ca2+-dependent K+ (KCa) channels, generating spontaneous transient outward currents (STOCs).
  • STOCs hyperpolarize arterial myocytes, reducing Ca2+ influx and promoting vasodilation.

Purpose of the Study:

  • To investigate the role of protein kinase C (PKC) in modulating Ca2+ spark and STOC frequency.
  • To determine the impact of PKC activation on KCa channel activity and arterial myocyte membrane potential.

Main Methods:

  • Used PKC activators (phorbol 12-myristate 13-acetate and 1,2-dioctanoyl-sn-glycerol) to modulate Ca2+ spark and STOCs in arterial myocytes.

Related Experiment Videos

  • Measured Ca2+ spark frequency and STOCs, including amplitude and frequency.
  • Assessed SR Ca2+ content using caffeine-induced Ca2+ transients and evaluated KCa channel open probability.

    • Main Results:

    • PKC activators significantly decreased Ca2+ spark frequency (by 72% and 60%).
    • PMA reduced STOC frequency by 83% and amplitude by 22%.
    • Reduced STOC frequency was independent of SR Ca2+ depletion and voltage-dependent Ca2+ channel blockade.

    Conclusions:

    • PKC activation modulates Ca2+ spark frequency, likely via an effect on RyR channels.
    • This modulation leads to decreased STOC frequency and KCa channel activity.
    • PKC-mediated regulation of Ca2+ sparks offers a potential mechanism for controlling arterial tone and vasodilation.