Nifedipine and BAY K inhibit contraction independently from their action on calcium channels.
Voltage-clamp experiments were performed on twitch skeletal muscle fibres in a double sucrose-gap device in order to investigate the effect of 1,4-dihydropyridines (DHP) on excitation-contraction coupling during 50 ms step depolarizations. External solution used was free of permeant anions and contained only Ca++ as permeant cation. It is shown that in these conditions Nifedipine (a Ca++ channel antagonist) and BAY K 8644 (a Ca++ channel agonist) inhibit contraction in a way independent of their action on the gating of tubular calcium channels. These results indicate also that a close relation between DHP receptors and calcium channels must be taken with caution.
Jacquemond
V
V
Laboratoire de Physiologie des Eléments Excitables (CNRS UA 244), Université Claude Bernard, Villeurbanne, France.
Rougier
O
O
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D007473:Ion Channels / Q000187:drug effects*; D008564:Membrane Potentials / Q000187:drug effects; D009119:Muscle Contraction / Q000187:drug effects*; D009543:Nifedipine / Q000494:pharmacology*; D011893:Rana esculenta
D007473:Ion Channels; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D009543:Nifedipine; D002118:Calcium