Alpha 2-adrenoceptor-mediated autoinhibition of sympathetic transmitter release in guinea-pig vas deferens studied by intracellular and focal extracellular recording of junction potentials and currents.

Excitatory junction potentials (e.j.ps; intracellular electrodes) and excitatory junction currents (e.j.cs; extracellular electrodes) elicited by stimulation (20 pulses at 1 Hz every minute) of the hypogastric nerve trunk were recorded from guinea-pig isolated vas deferens. Intracellular recording. At a variety of stimulation intensities, bath-applied yohimbine (0.1-1 mumol/l) did not change the first one to three e.j.ps in a train but increased the amplitude of subsequent e.j.ps. The effect of yohimbine was abolished in tissues from reserpine-pretreated guinea pigs. Bath-applied desipramine (0.1 mumol/l) diminished the amplitude of all but the first one to three e.j.ps in a train.--Extracellular recording. Yohimbine (0.1-1 mumol/l), when applied locally through the recording suction electrode, increased the number of e.j.cs per given number of stimuli, i.e., enhanced the probability of occurrence of e.j.cs. When desipramine (0.1 mumol/l) was present both in the bath and in the recording electrode, the probability of the occurrence of e.j.cs was decreased. In the presence of desipramine, yohimbine (0.1-1 mumol/l) increased the number of e.j.cs even more markedly. Neither the nerve terminal impulse nor the number of spontaneous e.j.cs was changed by yohimbine. A mixture of tetraethylammonium (2 mmol/l) and 4-aminopyridine (0.2 mmol/l), when applied locally, both increased the number of e.j.cs and changed markedly the shape of the nerve terminal impulse.(ABSTRACT TRUNCATED AT 250 WORDS)