Effect of slow calcium channel blockers on the electromechanical activity of frog myocardium in the presence of epinephrine

Gen Physiol Biophys. 1985 Aug;4(4):349-58.

Abstract

The calcium channels blockers fenihidine (3.5 X 10(-5) mol/l), ryosidine (10(-5) mol/l), D-600 (10(-5) mol/l) and Mn ions (2 X 10(-3) mol/l or 5 X 10(-3) mol/l) block contraction force and shorten the duration of action potentials of the frog myocardial ventricle strand under normal conditions. When contraction force and the duration of action potentials were restored by epinephrine (10(-5) mol/l), these agents were unable to suppress these parameters. The increase in both contraction force and the duration of action potentials induced by epinephrine were blocked by acetylcholine. Recording by voltage clamp of inward calcium current (Ica) of the frog atrial trabeculae it was found that fenihidine decreases Ica activated by epinephrine to a smaller extent than observed at normal conditions. Let as assume that epinephrine increases Ica by means of increasing number of calcium channels so these data support the proposed existence of as many as two calcium channel fractions in frog myocardium, which differ in the sensitivity to calcium channels blockers.

MeSH terms

  • Action Potentials / drug effects
  • Animals
  • Calcium Channel Blockers / pharmacology*
  • Epinephrine / pharmacology*
  • Gallopamil / pharmacology
  • Heart / drug effects
  • Heart / physiology*
  • In Vitro Techniques
  • Manganese / pharmacology
  • Myocardial Contraction / drug effects
  • Nifedipine / pharmacology
  • Organic Chemicals
  • Ranidae
  • Tetrodotoxin / pharmacology
  • Ventricular Function

Substances

  • Calcium Channel Blockers
  • Organic Chemicals
  • Gallopamil
  • Manganese
  • Tetrodotoxin
  • ryosidine
  • Nifedipine
  • Epinephrine