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Phosphorylation shifts the time-dependence of cardiac Ca++ channel gating currents

I R Josephson1, N Sperelakis

  • 1Department of Physiology and Biophysics, University of Cincinnati, College of Medicine, Ohio 45267-0576.

Biophysical Journal
|August 1, 1991
PubMed

Insights

Neurotransmitters regulate ion channels via cyclic AMP-dependent phosphorylation. This study shows beta-adrenergic stimulation speeds cardiac calcium channel gating charge movement, suggesting a mechanism for altered calcium currents.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cardiology

Background:

  • Neurotransmitters physiologically regulate ion channel activity through cyclic AMP-dependent phosphorylation.
  • Channel phosphorylation alters opening probability and voltage dependence.
  • Voltage dependence is governed by the channel's voltage-sensing moiety charge movement.

Purpose of the Study:

  • To investigate the effect of beta-adrenergic stimulation on cardiac calcium channels.
  • To elucidate the role of gating charge movement in altered calcium channel kinetics and voltage dependence.

Main Methods:

  • Studied the gating charge movement of cardiac Ca++ channels.
  • Applied isoproterenol and cAMP to induce channel phosphorylation.

Main Results:

  • Isoproterenol or cAMP significantly speeds the kinetics of Ca++ channel gating charge movement.
  • These kinetic changes in charge movement correlate with observed changes in cardiac calcium currents.

Conclusions:

  • Beta-adrenergic stimulation initiates changes in cardiac calcium currents partly through parallel alterations in gating charge movement.
  • Phosphorylation of cardiac calcium channels by beta-adrenergic agents affects their gating charge kinetics.

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