Effects of ephedrine on the neuromuscular transmission in vitro

In isolated rat phrenic nerve-diaphragm preparations, ephedrine (80μmo\l L) antagonized the neuromuscular paralysis induced by high K+ depolarization. This excitatory effect of ephedrine was blocked by propranolol (1μmol/L). The fact that pretreatment with reserpine did not affect the action of ephedrine indicated that this action was probably not involved in released catecholamines. Ephedrine (1 mmoI/L) slightly and temporarily augmented the twitch response of diaphragm to the electric stimulation of phrenic nerve. At higher concentrations (3-10 mmol/L), ephedrine inhibited the twitch response in a concentration-dependent manner. The inhibitory effect of ephedrine was not antagonized by either propranolol or phentolamine. Ephedrine did not change the resting membrane potential of rat diaphragm muscle cells significantly, Ephedrine 1 mmol/L increased mepp frequency temporarily, 7 mmol/L markedly decreased the mepp amplitude and abolished it finally. Ephedrine (l mmol/L) increased the quantal content of epp at first, and then decreased. At 5 mmol/L, ephedrine decreased the quantal content rapidly. 4-Aminopyridine partially antagonized the inhibitory effect of ephedrine on the neuromuscular junction, and restored the epp which has been abolished by ephedrine. These results suggest that the augmentative action of ephedrine at 1 mmol/L on the twitch response to indirect stimulation maybe related to its presynaptic action. The inhibitory action of ephedrine on neuromuscular transmission is a direct action at neuromuscular junction that is independent of adrenoceptors, and involves both presynaptic and postsynaptic actions.