EFFECTS OF SEVERAL ANTICHOLINERGIC DRUGS ON THE POST-TETANIC POTENTIATION IN THE PHRENIC NERVE-DIAPHRAGM PREPARATION OF THE RAT

摘要

References(28) Cited-By(5) The phenomenon of the post-tetanic potentiation (PTP) has been reported to occur in the neuromuscular junction, which generally refers to a long lasting increased response following the tetanic stimulation (1-5). There are considerable divergences of opinions with respect to a mechanism of PTP, which have been briefly reviewed in the previous paper (6). However, it seems to us that a generally accepted view for it is that PTP is explained in terms of the potentiation of transmitter release per nerve stimulation following the tetanic stimulation. This potentiation have been attributed to an increase in the amplitude of the pre-synaptic spike potential due to hyperpolarization of the nerve terminals (7), mobilization of transmitter (3), an intracellular accumulation of the sodium ion in the nerve terminals (8) and some change in the ionized calcium at a membrane site important in transmitter release (9, 10). On the other hand there are many p a pers (11-17) dealing with pharmacological properties of the pre-synaptic terminals. Langley and Kato (18), later Masland and Wigton (19), found that curare, at a dose not enough to block the neuromuscular transmission, abolished both the twitch tension and the nerve repetitive discharge produced by administrations of ChE inhibitors. Recently Standaert (15, 16) has reported that a dose of d-tubocurarine or succinylcholine, having no appreciable effects on the twitch tension, abolished the post-tetanic repetitive activity in the cat soleus nerve which is a nerve phenomenon. In the present experiments in order to elucidate the mechanism of PTP effects of anticholinergic drugs on PTP were examined, especially, at a dose having no appreciable effects on the pre-tetanic twitch tension. A preliminary report of some parts of the present experiments has been published in This journal (20).