Abstract
PGE1and PGE2reversibly and dose‐dependently inhibited transmitter release from the stimulated guinea pig vas deferens. The two compounds proved equiactive and more prone to inhibit transmitter release at a low than at a high stimulation frequency. The PGEs inhibited the twitch response but produced inconsistent effects on contractions induced by prolonged stimulation. The difference may be due to the fact that the PGEs reduce the excitatory junction potentials and depolarize the effector cell membrane. Phenoxybenzamine increased transmitter release in response to nerve stimulation but failed to significantly alter the inhibitory effect of PGE2. It is therefore concluded that PGEs and presumed presynoptic α‐receptors probably intrude upon different levels of the process of excitation secretor, coupling. A possible model for the action of locally formed PGEs on the neuromuscular transmission of the vas deferens is advanced.