1. Intracellular microelectrode recording techniques were used to investigate the action of the putative P2-purinoceptor antagonist, suramin, on sympathetic neurotransmission in the guinea-pig isolated vas deferens. 2. The resting membrane potential of the control cells was 67.4 +/- 0.7 mV (n = 48). Field stimulation of the sympathetic nerves innervating the vas deferens produced excitatory junction potentials (e.j.ps) which reached a mean magnitude of 8.5 +/- 0.8 mV (n = 23) when fully facilitated at a stimulation frequency of 0.5 Hz. 3. Introduction of suramin 1-100 microM produced no change in the resting membrane potential of the smooth muscle cells, but gradually reduced e.j.p. magnitude. Suramin, 20 microM, reduced the mean magnitude of the fully facilitated e.j.ps to 1.4 +/- 0.3 mV (n = 18). 4. After suramin-induced inhibition of e.j.ps, nerve stimulation at 1-8 Hz resulted in summation of e.j.ps to a subthreshold level. Subsequent introduction of the alpha-adrenoceptor antagonists, prazosin or phentolamine (1 microM) did not reduce the magnitude of the summated e.j.ps. 5. The results support the proposal that e.j.ps in vas deferens are mediated by adenosine 5'-triphosphate, and not by noradrenaline, and confirm that suramin can antagonize responses mediated via P2-purinoceptors.