The large conductance voltage‐ and Ca2+‐activated K+ (BK or KCa1.1) channel is a key player in controlling excitability and contractility of animal urinary bladder smooth muscle (UBSM), however its role in human UBSM is unknown. Here, using the BK channel specific inhibitor‐iberiotoxin, functional studies and the perforated patch‐clamp technique, we identified the BK channel in human UBSM. In isolated UBSM strips iberiotoxin increased spontaneous phasic contraction amplitude and force (n=10). In isolated UBSM cells, voltage‐step depolarizations caused large K+ currents (∼1 nA; n=15). About 80% of these K+ currents were inhibited by iberiotoxin. In the voltage range of −40 to +40 mV, these cells also revealed spontaneous transient outward currents (STOCs). STOCs amplitude and frequency increased with increasing the holding potential toward positive values (n=20). STOCs were inhibited by iberiotoxin (n=4). In the presence of ryanodine, when the STOCs were blocked, single channels with large single channel conductance (120.6 pS) were observed (n=10). Their amplitude and open probability were voltage‐dependent. In current‐clamp mode, iberiotoxin caused membrane potential depolarization (n=4). The data reveal that the BK channel is the major voltage‐dependent K+ channel expressed in human UBSM cells that plays a key role in determining cell excitability and contractility. Supported by DK070909 to G.V.P.