Bradykinin, (BK) an inflammatory mediator, which can cause bronchoconstriction. In this study, we investigated the membrane currents induced by BK in cultured human airway smooth muscle (ASM) cells. Depolarisation of the cells induced outward currents, which were inhibited by TEA in a concentration dependent manner with an IC50 of 0.33 µM. The currents were increased by elevating intracellular free Ca²⁺ concentration, suggesting they are calcium-activated potassium channels I_k(Ca). Pre-exposure to inhibitor of I_k(Ca) of large conductance (BKCa), iberiotoxin, and small conductance (SKCa), apamin, inhibited the increase of outward current induced by BK. The relative contribution of BKCa was greatest in early passage cells. Both nickel and SKF96365 (10 µM) inhibited the increase of the I_k(Ca) induced by BK, however, the L-type Ca²⁺ channel blocker, nifedipine had no effect. Activation of the BK-induced current was inhibited by heparin, indicating dependece on intact IP3-sensitive intracellular Ca²⁺ stores. BK also increased inositol phosophate accumulation and induced a transient Ca²⁺-activated chloride current (CACC) and a sustained non-selective cation current I_CAT. In summary BK activates BKCa, SKCa, CACC and I_CAT via IP3 sensitive stores in human ASM.