BK channels are large unitary conductance K⁺ channels cooperatively activated by intracellular calcium and membrane depolarisation. We show that BK channels regulate electrical activity in β‐cells of mouse pancreatic islets exposed to elevated glucose. In 11.1 mm glucose, the non‐peptidyl BK channel blocker paxilline increased the height of β‐cell action potentials (APs) by 21 mV without affecting burst‐ or silent‐period durations. In isolated β‐cells, paxilline increased AP height by 16 mV without affecting resting membrane potential. In voltage clamp, paxilline blocked a transient component of outward current activated by a short depolarisation, which accounted for at least 90% of the initial outward K⁺ current. This BK current (I_BK) was blocked by the Ca²⁺ channel blockers Cd²⁺ (200 μm) or nimodipine (1 μm), and potentiated by FPL‐64176 (1 μm). I_BK was also 56% blocked by the BK channel blocker iberiotoxin (100 nm). I_BK activated more than 10‐fold faster than the delayed rectifier I_Kv over the physiological voltage range, and partially inactivated. An AP‐like command revealed that I_BK activated and deactivated faster than I_Kv and accounted for 86% of peak I_K, explaining why I_BK block increased AP height. A higher amplitude AP‐like command, patterned on an AP recorded in 11.1 mm glucose plus paxilline, activated 4‐fold more I_Kv and significantly increased Ca²⁺ entry. Paxilline increased insulin secretion in islets exposed to 11.1 mm glucose by 67%, but did not affect basal secretion in 2.8 mm glucose. These data suggest a modified model of β‐cell AP generation where I_BK and I_Kv coordinate the AP repolarisation.