Relationship of ion channel activity to control of myometrial calcium.

This article reviews the contribution of ion channels to membrane potential, the ion channels expressed in myometrium, and the effect of ion channel activity on the control of myometrial intracellular free calcium. Plasma membranes constitute barriers to permeability that establish concentration gradients of ions inside versus outside the cell. Na+, CA2+, and Cl- are normally in higher concentration outside than inside cells, whereas K+ is higher inside. In myometrium, Ca2+ entry into cells mediates myometrial membrane potential changes and serves as the internal signal for contraction. K+ efflux is thought to promote repolarization after an action potential and to participate in setting the resting membrane potential. Ions cross the cell membrane through channels that have different regulated properties and selectivities. Ion movement has been measured by a number of techniques, including radiolabeled ion flux, use of intracellular indicators, and patch-clamp methodology. A number of myometrial Ca2+ channels have been described, including voltage-regulated L-type channels and Ca2+ entry in response to intracellular Ca2+ store depletion. Fast Na+ channels may contribute to cation entry late in pregnancy. K+ channels in myometrium include Ca(2+)-activated channels, a delayed rectifier, and an inward rectifier. A Ca(2+)-activated Cl- channel is also present in myometrium. In addition to being regulated by Ca2+, the activity of a number of these channels can be regulated by uterine contractants and relaxants. Regulation of ion channel activity can affect intracellular free Ca2+ concentrations in the myometrium. Therefore, control of ion channel activity represents one of several approaches for controlling myometrial contractile activity.