Abstract
The MaxiK channel is the large-conductance, voltage-dependent, and Ca2+-activated K+ channel. This channel is almost ubiquitously distributed among mammalian tissues including smooth muscles. The ability of MaxiK to work as a rheostat fine tuning membrane potential and intracellular Ca2+ enables it to mediate opposite functions: it facilitates contraction, but also acts as a negative feedback mechanism to restore tone after a contraction cycle. MaxiK activation mediates relaxations to a variety of physiological substances, whereas its inhibition plays a significant role in contractile responses. At the molecular level, MaxiK is a protein complex formed by at least two integral dissimilar membrane subunits, the pore-forming α-subunit and a regulatory β-subunit. In smooth muscles, β1 is the predominant subunit and most MaxiK seem to be assembled of α- and β1-subunits. The presence of the β1-subunit confers MaxiK with higher Ca2+/voltage sensitivity, which makes this channel an efficient tuner of smooth muscle functions in physiological conditions. The enhanced smooth muscle mechanical activities in mice lacking the β1-subunit gene support the principal role of this channel molecular component in tissue and whole animal functions. In this review, we discuss MaxiK channel roles as a tuner of smooth muscle contractility, especially focusing attention on the modulatory β1-subunit.
