Figure 9. Mechanisms of BK‐elicited Ca²⁺ signal generation in PSCs .

A and B, removal of external Ca²⁺ has no effect on the initial [Ca²⁺]_i rise evoked by BK (1 nm, P > 0.7), but abolishes the following plateau phase (P < 0.0003). Readmitting external Ca²⁺, in the absence of BK stimulation, causes a transient rise in [Ca²⁺]_i. C, when the SERCA pump inhibitor CPA (20 μm) is present, the [Ca²⁺]_i rise upon readmission of external Ca²⁺ is prolonged. D, 2‐APB (100 μm) (IP₃R antagonist and inhibitor of CRAC channels) blocks Ca²⁺ signalling elicited by BK (1 nm). E, the CRAC channel blocker GSK‐7975A (10 μm) reduces markedly the plateau phase of the BK‐ (1 nm) elicited response (P < 0.0015). Washout of GSK‐7975A partially restored the response (P <  0.009). F, GSK (10 μm) does not inhibit the initial BK‐elicited Ca²⁺ signal occurring in the absence of external Ca²⁺ but prevents the [Ca²⁺]_i rise normally occurring upon external Ca²⁺ readmission. G, caffeine (30 mm) reversibly blocks BK‐ (1 nm) elicited Ca²⁺ signal. H, the phospholipase C inhibitor U73122 (30 μm) abolished Ca²⁺ signal generation elicited by BK (1 nm), both peak (P < 0.0002) and plateau (P < 0.00001).