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Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling
08:29

Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling

Published on: August 1, 2016

Regulation of cardiac Ca(2+) channel by extracellular Na(+)

Shahrzad Movafagh1, Lars Cleemann, Martin Morad

  • 1Department of Pharmacology, Georgetown University Medical Center, Washington, DC 20007, USA.

Cell Calcium
|February 26, 2011
PubMed

Insights

Hyponatremia, or low serum sodium, directly suppresses cardiac function by reducing calcium channel current. This finding offers a mechanism for poor cardiovascular outcomes in patients with low sodium levels.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Electrophysiology

Background:

  • Hyponatremia is linked to adverse cardiovascular outcomes, particularly in acute myocardial infarction and heart failure.
  • The precise mechanisms by which hyponatremia impairs cardiac function remain unclear.

Purpose of the Study:

  • To investigate the direct effects of low serum sodium on cardiac calcium channel function.
  • To elucidate the molecular mechanisms underlying sodium's modulation of calcium currents in the heart.

Main Methods:

  • Utilized voltage-clamped rat ventricular myocytes and HEK 293 cells expressing L-type calcium channels.
  • Manipulated extracellular sodium concentrations and assessed calcium channel current (I(Ca)) responses.
  • Investigated the influence of substituting monovalent ions, channel phosphorylation, and Na+/Ca2+ exchanger activity.

Main Results:

  • A 15mM reduction in extracellular sodium suppressed calcium channel current by approximately 15%.
  • Maximal suppression of ~30% was observed when sodium levels dropped to 100mM or less.
  • The effect was partially dependent on the substituting ion and independent of channel phosphorylation or Na+/Ca2+ exchanger activity. Acidification enhanced the suppressive effect of sodium withdrawal.

Conclusions:

  • Low serum sodium directly down-regulates cardiac calcium channel current.
  • Sodium and potentially hydrogen ions may interact with the calcium channel pore, modulating divalent ion flux.
  • This provides a direct mechanistic link between hyponatremia and impaired cardiac contractility.

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