Myometrial cells are phenotypically modified to a non-contractile state during the activation phase. According to Cunningham et al. (2018), natural stimuli are not effective for uterine muscle response, and such myometrial unresponsiveness lasts until the end of pregnancy. Anderson and Avery (2019) say about myometrical excitability and spontaneous activity. Estrogen provokes the express of receptors for prostaglandins and oxytocin or muscle fibers communication because of gap junctions.
During the stimulation phase, the influence of oxytocin considerably increases. Estrogen initiates expression of oxytocin genes, which results in muscle contractions and active labor. The increased number of oxytocin in the myometrial cell membranes promotes labor and mechanical stretch (Anderson & Avery, 2019). As soon as labor is initiated, myometrial activity (contraction and relaxation) continue via the enzymatic phosphorylation and other interactions. Prostaglandins are responsible for uterine contractile activity as well.
Uterine contraction is a unique mechanism when uterine muscle cells are shortened. This intermittent process (mechanical stretch and hormone-receptor binding) allows reperfusion of the uterine muscle, placenta, and fetus (Anderson & Avery, 2019). First, the myosin head is attached to the site, and then recharging occurs when the myosin head binds to an adenosine triphosphate (ATP) molecule. The cleft closes around ATP to be hydrolyzed to adenosine diphosphate (ADP) on the actin filament, which causes contraction.