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Calcium-sensitive delayed rectifier potassium current in guinea pig ventricular cells.

N Tohse1

  • 1National Institute for Physiological Sciences, Okazaki, Japan.

The American Journal of Physiology
|April 1, 1990
PubMed
Summary

Calcium ions enhance the delayed rectifier potassium current (IK) in guinea pig heart cells. This calcium sensitivity likely increases the number and open probability of functional IK channels, impacting cardiac function.

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Area of Science:

  • Cardiovascular Physiology
  • Electrophysiology
  • Ion Channel Function

Background:

  • The delayed rectifier potassium current (IK) is crucial for cardiac repolarization.
  • Understanding the regulation of IK by intracellular calcium ([Ca2+]i) is vital for cardiac health.

Purpose of the Study:

  • To investigate the calcium sensitivity of the delayed rectifier potassium current (IK) in guinea pig ventricular cells.
  • To elucidate the mechanism by which intracellular calcium modulates IK.

Main Methods:

  • Whole-cell patch-clamp technique with cell dialysis in guinea pig single ventricular cells.
  • Ensemble noise analysis to study functional IK channel properties.

Main Results:

  • IK increased significantly with intracellular calcium concentrations ([Ca2+]i) from 10(-8) M (pCa 8) to 10(-7) M (pCa 7).

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  • Intracellular calcium elevation increased the number and open probability of functional IK channels, without altering unit amplitude.
  • IK activation and deactivation time constants were minimally affected, but amplitude components were modulated.

    • Conclusions:

    • Intracellular calcium enhances the delayed rectifier potassium current (IK) in cardiac cells.
    • This enhancement is likely mediated by an increase in the number and open probability of functional IK channels.
    • Calcium-sensitive IK in cardiac cells differs from calcium-activated K+ currents in other tissues due to distinct activation properties and single-channel conductance.