Intracellular microelectrode recording was used to examine the effects of suramin, a P2-purinoceptor antagonist, on the electrical responses evoked by sympathetic nerve stimulation in the rat isolated tail artery. Field stimulation (10 or 20 pulses at 0.5, 1 and 2 Hz) evoked a biphasic electrical response, consisting of fast, transient excitatory junctional potentials (e.j.p.s) and a slow, prolonged depolarisation. Suramin (100 microM) abolished the e.j.p.s and significantly increased the amplitude of the slow depolarisation at all frequencies. In contrast, phentolamine (2 microM) abolished the slow depolarisation, but had no effect on the magnitude of e.j.p.s. Neither drug altered the resting membrane potential of cells. The ability of suramin to inhibit e.j.p.s in rat tail artery is consistent with the proposal that it is a P2X-purinoceptor antagonist and supports a role for ATP as an excitatory cotransmitter from the sympathetic nerves innervating this tissue. Suramin is also able to increase the alpha-adrenoceptor-mediated slow depolarisation by an unknown mechanism.