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

Abstract

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.