Figure 3.

(A) A dissection of the various ion channels responsible for depolarization, repolarization and hyperpolarization of the cell membrane during an action potential event in a urethral smooth muscle cell.^30,31 Under control conditions the BK_Ca channel is primarily responsible for reducing the duration of the action potential spike and hyperpolarizing the membrane potential; K_v2 channels do not contribute to this process.³⁰ When BK_Ca channel current is suppressed, K_v2 channels are involved in repolarizing the membrane potential. When both BK_Ca and K_v2 channel currents are suppressed it is not yet known which conductances repolarize and stabilize the membrane potential. The conductances responsible for setting and maintaining/stabilizing the resting membrane potential have also not been reported. (B) An illustration of membrane currents evoked from a urethral smooth muscle cell in response to a step voltage clamp pulse. Depolarization of the cell membrane results in an L-type VGCC inward current. A rapidly activating, transient outward current is evident, carried by BK_Ca channels that requires VGCC activity and CICR from the SR. This is followed by a sustained and “noisy” outward current also carried by BK_Ca channels.^30,31,40 The delayed-rectifier K_v2 current can be observed when BK_Ca channel current is inhibited. Inhibition of both BK_Ca and K_v2 channel currents leaves a small net outward current that has not been fully resolved. Abbreviations: L-type VGCCs, long-lasting voltage-gated Ca²⁺ channels; ? Channels, unknown channels; BK_Ca, large conductance, Ca²⁺-activated K⁺ channel; K_v2, voltage-gated K⁺ channels (Shab-related subfamily); mV, millivolt; ms, millisecond; RMP, resting membrane potential.