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Tetrodotoxin blockade on canine cardiac L-type Ca²⁺ channels depends on pH and redox potential

Bence Hegyi1, István Komáromi, Kornél Kistamás

  • 1Department of Physiology, University of Debrecen, P.O. Box 22, H-4012 Debrecen, Hungary.

Marine Drugs
|June 18, 2013
PubMed

Insights

Tetrodotoxin (TTX) blocks cardiac L-type calcium channels, contrary to its known action on sodium channels. Its potency is influenced by pH and redox conditions, suggesting a specific binding site.

Area of Science:

  • Cardiology
  • Pharmacology
  • Channel Physiology

Background:

  • Tetrodotoxin (TTX) is a well-established blocker of voltage-gated sodium channels.
  • Recent findings suggest TTX can also inhibit L-type calcium current (I(Ca)) in cardiac cells.

Purpose of the Study:

  • To investigate the TTX-sensitivity of cardiac L-type calcium current (I(Ca)).
  • To examine the influence of channel phosphorylation, extracellular pH, and redox potential on TTX's effect on I(Ca).

Main Methods:

  • Whole-cell voltage clamp technique on isolated canine ventricular myocytes.
  • Systematic variation of extracellular pH (acidic vs. alkaline).
  • Manipulation of bathing medium redox potential (reductant vs. oxidant).
  • Assessment of TTX inhibition under basal and forskolin-induced phosphorylation conditions.

Main Results:

  • TTX exhibited significantly greater inhibition of I(Ca) in acidic (pH 6.4) compared to alkaline (pH 8.4) conditions.
  • TTX was more potent in blocking I(Ca) in a reductant milieu than in an oxidant milieu.
  • Channel phosphorylation by forskolin did not alter the inhibitory potency of TTX.

Conclusions:

  • The TTX-sensitivity of cardiac L-type Ca channels is modulated by extracellular pH and redox state.
  • These findings support a model where TTX binds to the selectivity filter of cardiac L-type Ca channels.
  • TTX's interaction with cardiac calcium channels warrants further investigation in electrophysiology and pharmacology.

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