Intracellular recordings were obtained from neurones of the guinea-pig submucous plexus. Inhibitory synaptic potentials (i.p.s.p.s) were compared with hyperpolarizations evoked by brief, local applications of noradrenaline and by superfusion with adrenoceptor agonists. Hyperpolarizing potentials elicited by brief applications of noradrenaline were similar to the i.p.s.p. in latency of onset, amplitude, time course, conductance increase, reversal potential and ionic dependence. Both responses were blocked by low concentrations of Ba2+ and quinine. 6-hydroxydopamine selectively and irreversibly abolished the i.p.s.p. and resulted in a complete loss of catecholamine fluorescent nerve fibres in the submucous plexus. The alpha 2-adrenoceptor antagonists, phentolamine, yohimbine and RX781094, reversibly blocked the i.p.s.p. and the noradrenaline hyperpolarization. Prazosin, propranolol, atropine and naloxone had no effect on these responses. Superfusion with noradrenaline and clonidine produced dose-dependent membrane hyperpolarizations. Noradrenaline and clonidine dose-hyperpolarization curves were shifted to the right in a parallel fashion by alpha 2-adrenoceptor antagonists. Determination of the dissociation equilibrium constants for phentolamine, yohimbine and RX781094 showed that the hyperpolarization produced by noradrenaline perfusion is due to alpha 2-adrenoceptor activation. It is concluded that the release of noradrenaline from sympathetic nerves activates post-synaptic alpha 2-adrenoceptors, resulting in the K+ conductance increase which underlies the i.p.s.p. in submucous plexus neurones.