Physiology of myometrial function: intercellular coupling and its role in uterine contractility

Abstract

The mammalian uterus is composed of a preponderance of small smooth muscle cells usually aligned in two layers. The number of muscle cells in the human uterus at term is estimated at 200 billion, each minute fusiform cell measuring about 5–10μm in diameter and about 200μm in length. The main function of the uterus is to harbour the developing fetus during pregnancy and then to contract vigorously during labour to expel the products of conception. In order for the uterus to contract rhythmically and forcefully, a mechanism must exist to allow interaction between muscle cells in order to achieve synchronous activity. Phasic or cyclical patterns of contractile activity of the uterus cannot be accounted for by stimulation or inhibition from the nervous or endocrine systems. Since myometrial cells are dependent upon action potentials for their contractile processes, some system must be present between the muscle cells for the propagation of action potentials between them. The observation that gap junctions occur in large numbers between myometrial cells during parturition is thought to be significant in this regard and they are considered to play an essential role in parturition and in the control and co-ordination of uterine contractility. In this brief review, we will discuss the role of gap junctions in the modulation of myometrial contractility and the mechanisms that regulate their synthesis and permeability.