An electrophysiological study of presynaptic alpha-adrenoceptors in the vas deferens of the mouse.

1--Effects of clonidine and alpha-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 microM, 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 microM, rauwolscine 1 microM and corynanthine 1 microM di 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 microM was much less effective than yohimbine 1 microM or rauwolscine 1 microM, and corynanthine 0.1 microM had no effect. 4--Clonidine 0.01 microM reduced the e.j.p. amplitudes evoked by single pulses and its effect was counteracted by yohimbine 1 microM. 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 microM did not further increase the e.j.p. amplitudes in these organs, whereas clonidine 0.01 microM 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 alpha-adrenoceptors, and that these receptors are normally activated by neurally released noradrenaline.