The negative chronotropic effect of Cs(+) ions on generation of transmembrane potentials in mouse sinoatrial node

M A Gonotkov1, V A Golovko

  • 1Institute of Physiology, Komi Research Centre, Urals Division of Russian Academy of Sciences, Syktyvkar, Russia.

Insights

Cesium ions (Cs+) significantly slow heart rate by blocking the I(f) current in mouse sinoatrial node cells. This effect, observed at 1 mM Cs+, reversibly reduces action potential generation, impacting heart rhythm regulation.

Area of Science:

  • Cardiology
  • Electrophysiology
  • Pharmacology

Background:

  • The sinoatrial (SA) node generates the heart's electrical impulses.
  • The hyperpolarization-activated current, I(f), plays a crucial role in SA node pacemaking.
  • Understanding I(f) current blockade is key to modulating heart rate.

Purpose of the Study:

  • To investigate the chronotropic effects of cesium (Cs+) on the I(f) current in mouse SA node cells.
  • To determine the concentration-dependent effects of Cs+ on cardiac action potential parameters.
  • To elucidate the role of I(f) current in regulating the intrinsic heart rate.

Main Methods:

  • Experiments were conducted on spontaneously contracting heart strips from mouse SA nodes.
  • Varying concentrations of cesium (Cs+) were applied to assess its impact on electrical activity.
  • Measurements included diastolic depolarization duration, rate, and action potential duration.

Main Results:

  • 1 mM Cs+ caused a significant negative chronotropic effect, reducing diastolic depolarization duration by 75% and rate by 59%.
  • Action potential duration decreased by 29% with 1 mM Cs+.
  • Spontaneous action potential generation ceased at approximately 8.5 mM Cs+, with reversible effects observed.

Conclusions:

  • Cesium ions effectively block the I(f) current in mouse SA node cells.
  • I(f) current blockade by Cs+ significantly reduces the rate of action potential generation, by approximately 42%.
  • These findings highlight the critical role of I(f) current in cardiac pacemaking and suggest potential therapeutic targets for heart rate modulation.

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