In the field-stimulated mouse vas deferens the twitch inhibiting potency of prazosin (1 microM) and alpha,beta-methylene ATP (MeATP, 10 microM) was studied, using two types of stimulation-response curves, (a) variation of frequency from 3 to 100 Hz at a constant pulse width of 0.1 ms and (b) variation of pulse width from 0.04 to 0.8 ms at a constant frequency of 15 Hz. Prazosin and MeATP reduced the twitch response by eliminating the noradrenergic and purinergic component, respectively. After the combined application of both compounds a small third twitch component remained that was most prominent at high frequencies. Reserpinization reduced the effect of prazosin but enhanced that of MeATP and increased the cholinergic component. 6-Hydroxydopamine enhanced the effects of prazosin and MeATP to the same extent, but left the cholinergic component intact. In vasa pre-loaded with [3H]-noradrenaline, field stimulation induced a larger release of tritium at high frequency and short pulse duration (100 Hz, 0.1 ms) than at lower frequency and long pulse duration (15 Hz, 0.3 ms). Prazosin (1 microM) augmented both the spontaneous and the stimulation-induced overflow of tritium, whereas MeATP (10 microM) had only a negligible negative effect on the outflow of label. In conclusion, the twitch contraction of the mouse vas deferens has a small cholinergic component in addition to the noradrenergic and purinergic components. Adrenergic and purinergic transmission seem not to run strictly in parallel: the purinergic component dominates during stimulation at low frequency and long pulse duration, and after reserpinization; 4-aminopyridine enhances the adrenergic mechanism more than the purinergic one.