Abstract
The site and mode of the muscle relaxing action of phenethylguanidine (PG), one of the guanidine derivatives, were studied electrophysiologically in the frog sciatic nerve sartorius preparation. In the indirectly stimulated muscle, the end-plate potential was reduced in amplitude without any change in the resting potential, and the twitch tension was completely blocked in the presence of PG in a concentration of 1.2×10-4g/ml. The amplitudes of the miniature endplate potentials and the iontophoretically produced ACh potentials were reversibly reduced with this concentration of PG. PG in a concentration less than 3.6×10-4g/ml did not cause any significant changes in electrical parameters of resting and active membranes in the nerve and muscle fibers. In the muscles treated with PG, addition of neostigmine caused a fall in twitch tension which was preceded by a small potentiation. Under this condition the amplitude of the end-plate potential was increased initially (first few minutes) but then followed by a progressive decline. The observations may be partly explained on the basis of a competitive receptor-blocking action of PG, but cannot be explained completely without assuming an additive non-competitive receptor-blocking action of drugs.
