Báo cáo khoa học: Inducible knockout mutagenesis reveals compensatory mechanisms elicited by constitutive BK channel deficiency in overactive murine bladder

The large-conductance, voltage-dependent and Ca 2+ -dependent K + (BK) channel links membrane depolarization and local increases in cytosolic free Ca 2+ to hyperpolarizing K + outward currents, thereby controlling smooth muscle contractility. Constitutive deletion of the BK channel in mice (BK )⁄ ) ) leads to an overactive bladder associated with increased intravesi-cal pressure and frequent micturition, which has been revealed to be a result of detrusor muscle hyperexcitability.