| Summary: | The large-conductance voltage- and Ca<sup>2+</sup>-activated K<sup>+</sup> channel (BK<sub>Ca</sub>) is an important regulator of membrane excitability in a wide variety of cells and tissues. In myometrial smooth muscle, activation of BK<sub>Ca</sub> plays essential roles in buffering contractility to maintain uterine quiescence during pregnancy and in the transition to a more contractile state at the onset of labor. Multiple mechanisms of modulation have been described to alter BK<sub>Ca</sub> channel activity, expression, and cellular localization. In the myometrium, BK<sub>Ca</sub> is regulated by alternative splicing, protein targeting to the plasma membrane, compartmentation in membrane microdomains, and posttranslational modifications. In addition, interaction with auxiliary proteins (i.e., β1- and β2-subunits), association with G-protein coupled receptor signaling pathways, such as those activated by adrenergic and oxytocin receptors, and hormonal regulation provide further mechanisms of variable modulation of BK<sub>Ca</sub> channel function in myometrial smooth muscle. Here, we provide an overview of these mechanisms of BK<sub>Ca</sub> channel modulation and provide a context for them in relation to myometrial function.
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