The action of bradykinin on neurons acutely isolated from airway parasympathetic ganglia of rats and its mechanism were investigated using the nystatin-perforated patch-clamp recording technique. Under current clamp conditions, an application of 0.1 microM bradykinin onto rat airway ganglion neurons induced a depolarization which was accompanied by the action potential firing. Bradykinin elicited inward currents with decreasing the membrane conductance when a ganglion neuron was held at a holding potential of -40 mV. The half-maximum effective concentration was 8.9 nM. The bradykinin response was mimicked by a B(2) receptor agonist, [Hyp(3)]-bradykinin, and was inhibited by HOE-140, a B(2) antagonist, suggesting the contribution of B(2) receptors. The bradykinin-induced inward current reversed at the K(+) equilibrium potential, which shifted 56.5 mV with a 10-fold change in extracellular K(+) concentration. The application of 10(-3) M Ba(2+) induced the inward current, and bradykinin failed to evoke a further inward current in the presence of Ba(2+). Bradykinin also reduced the amplitude of M-current deactivation induced by a hyperpolarizing step from a holding potential of -25 mV to -50 mV with a half-maximum effective concentration of 16 nM. Pretreatment with pertussis toxin had no effect on the bradykinin-induced inhibition of the M-current. From these results we suggest that bradykinin may be able to depolarize the airway parasympathetic ganglion neurons of rats associated with an inhibition of M-type K(+) channels through the B(2) type of bradykinin receptors.