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Nifedipine and BAY K inhibit contraction independently from their action on calcium channels

V Jacquemond1, O Rougier

  • 1Laboratoire de Physiologie des Eléments Excitables (CNRS UA 244), Université Claude Bernard, Villeurbanne, France.

Biochemical and Biophysical Research Communications
|May 16, 1988
PubMed

Insights

1,4-dihydropyridines affect skeletal muscle contraction independently of calcium channel gating. This suggests a cautious approach is needed when relating dihydropyridine receptors to calcium channels.

Area of Science:

  • Muscle Physiology
  • Pharmacology
  • Cellular Electrophysiology

Background:

  • Excitation-contraction coupling is crucial for muscle function.
  • 1,4-dihydropyridines (DHP) are known modulators of calcium channels.

Purpose of the Study:

  • To investigate the effect of DHPs on skeletal muscle excitation-contraction coupling.
  • To determine if DHP effects are mediated by direct action on calcium channels.

Main Methods:

  • Voltage-clamp experiments on twitch skeletal muscle fibers.
  • Utilized a double sucrose-gap device.
  • Employed a specialized external solution with Ca++ as the sole permeant cation.

Main Results:

  • Nifedipine (Ca++ channel antagonist) and BAY K 8644 (Ca++ channel agonist) inhibited contraction.
  • This inhibition occurred independently of their effects on tubular calcium channel gating.
  • Results challenge a direct link between DHP receptors and calcium channels.

Conclusions:

  • DHP action on skeletal muscle contraction is not solely dependent on calcium channel gating.
  • The relationship between DHP receptors and calcium channels requires further nuanced investigation.

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