There is evidence that noradrenaline enhances spontaneous contractions dose-dependently in guinea-pig antral circular muscle. To investigate the mechanism of this excitatory action, slow waves and membrane currents were recorded using conventional microelectrode techniques in muscle strips and the whole cell patch clamp technique in isolated gastric myocytes. On recording slow waves, noradrenaline (10^-5 M) induced the hyperpolarization of the membrane potential, although the shape of the slow waves became tall and steep. Also, spike potentiaIs occurred at the peaks of slow waves. These changes were completely reversed by administration of phentolamine (10^-5 M), an α-adrenoceptor blocker. Noradrenaline-induced hyperpolarization was blocked by apamin (10^-7 M), a blocker of a class of Ca²⁺ -dependent K⁺ channels. To investigate the mechanisms for these effects, we performed whole cell patch clamp experiments. Norndrenaline increased voltage-dependent Ca²⁺ currents in the whole range of test potentials. Noradrenaline also increased Ca²⁺ -dependent K⁺ currents, and this effects was abolished by apamin. These results suggest that the increase in amplitude and the generation of spike potentials on slow waves was caused by the activation of voltage-dependent Ca²⁺ channel via adrenoceptors, and hyperpolarization of the membrane potential was mediated by activation of apamin-sensitive Ca²⁺ -dependent K⁺ channels.