Mechanisms of Ca2+ Transport in Myometrium

Ca²⁺ are pivotal in controlling the contraction-relaxation process in smooth muscle, including myometrium. The energy-independent mechanisms of Ca²⁺ translocation in uterine smooth muscles have been investigated mainly by electrophysiological and pharmacological methods using intact muscles or isolated smooth muscle cell (SMC). There is much evidence indicating that the cell membrane of uterine SMC possesses Ca²⁺ channels that open upon depolarization to admit Ca²⁺. The major mechanism by which a large number of hormones and neurotransmitters stimulate Ca²⁺ influx in most visceral action potential-generating SMC is indirect activation of the voltage-operated Ca²⁺ channels by depolarization induced by opening of a nonselective receptor-operated channel that drives membrane potential toward the Na⁺ equilibrium potential. The hormonal status of the body along with different functional states is likely to affect Ca²⁺-transporting systems in uterine muscle. The dynamic characteristics of Ca²⁺ exchange of intact muscle have been shown to differ during pregnancy and postpartum.