Abstract Uterine smooth muscle is very similar to the smooth muscle of other visceral organs, but with a significant difference i.e. its contractile activity. During pregnancy, it is maintained in a quiescent state. Inefficient cell-to-cell coupling due to low level of expression of gap junctions and the inhibitory influence of nitric oxide are important factors responsible for minimal contractile activity in the uterine smooth muscle as gestation progresses. Labor is a state in which the uterus contracts frequently and forcefully to expel the products of conception. The instability of membrane potential of the uterine smooth muscle forms the basis for the spontaneity of contractions in the uterine smooth muscle. There occur changes in the calcium regulatory mechanisms that favor more forceful contractility of the muscle. A prerequisite for the effectiveness of these contractions is the ability of the myometrium to propagate its electrical activity, wherein lies the importance of gap junctions. Term of pregnancy is marked by a favorable estrogen: progesterone ratio and an upregulation of gap junctions, rendering the myometrium a functional syncitium. Superimposed on this enhanced activity and reactivity of the uterus is an array of uterine stimulants like prostaglandins and oxytocin, which, in the absence of uterine relaxants, result in forceful, well-sustained, rhythmic, and regular uterine contractions, and initiation of labor.