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Related Experiment Videos

Ca2+-induced current oscillations in rabbit ventricular myocytes

M A Laflamme1, P L Becker

  • 1Department of Physiology, Emory University School of Medicine, Atlanta, Ga. 30322, USA.

Circulation Research
|April 1, 1996
PubMed
Summary

Spontaneous calcium (Ca2+) oscillations in rabbit heart cells activate transient currents. These currents are primarily due to calcium-activated chloride (Cl-) channels, not cation channels, and may contribute to arrhythmias.

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Area of Science:

  • Cardiac Electrophysiology
  • Ion Channel Physiology
  • Molecular Cardiology

Background:

  • Spontaneous calcium (Ca2+) oscillations occur in ventricular myocytes.
  • These oscillations activate transient currents, but their ionic basis is not fully understood.
  • Potassium (K+) currents are often blocked in such experimental conditions.

Purpose of the Study:

  • To investigate the ionic mechanisms underlying transient currents activated by Ca2+ oscillations in rabbit ventricular myocytes.
  • To determine the contribution of different ion channels, specifically Na+-Ca2+ exchanger and Ca2+-activated Cl- channels, to these currents.

Main Methods:

  • Voltage clamp experiments on rabbit ventricular myocytes.
  • Manipulation of extracellular and intracellular ion concentrations (Cl-, Na+).

Related Experiment Videos

  • Induction of spontaneous Ca2+ transients via Na+-Ca2+ exchanger reversal and depolarization.

    • Main Results:

    • Transient currents were observed, reversing near the Cl- equilibrium potential under symmetrical Cl- conditions.
    • In the absence of Cl-, the current behaved like Na+-Ca2+ exchanger current.
    • In the absence of Na+, the current was identified as a Ca2+-activated Cl- current, reversing near the calculated Cl- equilibrium potential.

    Conclusions:

    • The study identifies a Ca2+-activated Cl- current as a significant component of transient currents in rabbit ventricular myocytes.
    • This Ca2+-activated Cl- conductance can carry inward current, potentially contributing to arrhythmogenic delayed afterdepolarizations in Ca2+-overloaded conditions.
    • No evidence for a Ca2+-activated cationic conductance was found.