Abstract
The present study describes the potentiating effect of dimorpholamine on twitch contraction of skeletal muscle and its mechanism on a cellular basis. Low concentrations (about 2×10-5 g/ml) of dimorpholamine potentiate the twitch contraction of frog sartorius muscle. In relatively high concentrations of 10-4-10-3 g/ml, however, the potentiation was followed by depression. Endplate potential was not affected by the drug. Dimorpholamine depolarized slightly the muscle membrane. The contracture tension vs. membrane potential relationship was hardly affected by the drug in the presence of 2×10-7 M tetrodotoxin. Action potentials recorded from muscle fibers treated with ethylene glycol showed marked and progressive increases in duration during exposure to the drug, and were finally blocked. It was concluded that twitch potentiation caused by dimorpholamine is due to the prolongation of the action potential. A likely molecular mechanism of this drug is discussed in terms of the kinetic model proposed by Adrian et al. (J. Physiol. 208, 607-644, 1970) for the excitable membrane of frog sartorius muscle.
