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An electrophysiological study of presynaptic α‐adrenoceptors in the vas deferens of the mouse

1 Effects of clonidine and α‐adrenoceptor antagonists were studied on sympathetic neuroeffector transmission in the mouse vas deferens. The amplitude of excitatory junction potentials (e.j.ps) was taken as a measure of transmitter release per impulse. 2 At a concentration of 0.5 μm, prazosin abolished depolarizations evoked by iontophoretically applied noradrenaline, but changed neither spontaneous nor nerve stimulation‐evoked e.j.ps. 3 Yohimbine 0.1 and 1 μm, rauwolscine 1 μm and corynanthine 1 μm did not change the e.j.p. amplitudes elicited by the first 2–3 pulses in trains of 15 pulses at 3 Hz, but increased the e.j.ps elicited by the subsequent pulses. Corynanthine 1 μm was much less effective than yohimbine 1 μm or rauwolscine 1 μm, and corynanthine 0.1 μm had no effect. 4 Clonidine 0.01 μm reduced the e.j.p. amplitudes evoked by single pulses and its effect was counteracted by yohimbine 1 μm. 5 In vasa deferentia from reserpine‐treated mice the e.j.p. trains were changed in much the same way as by yohimbine and rauwolscine. Yohimbine 1 μm did not further increase the e.j.p. amplitudes in these organs, whereas clonidine 0.01 μm caused a marked inhibition. 6 It is concluded that the release of the motor transmitter in the mouse vas deferens is inhibited by activation of presynaptic α‐adrenoceptors, and that these receptors are normally activated by neurally released noradrenaline.