In this review we discuss our current understanding of the cellular basis of uterine contractility, highlighting those areas requiring further study. It is clear that the basic processes of excitation-contraction coupling lie within the myometrial cell, and that these may be modified by agonists. In particular, the contribution of calcium homeostatic pathways to the control of human myometrial contractility during gestation will be discussed. Maturation of the hypothalamic-pituitary adrenal axis occurs prematurely in response to stimuli such as stress. This provides the stimulus to the onset of parturition. Another pathways are- release of endothelin production from uteroplacental vessels or- decidual activation and production of interleukin-1, tumour necrosis factor - α and epidermal growth factor- which enhance prostaglandin production in both the amnion and chorion, and also in the myometrium. A substantial increase of eicosanoids concentration in myometrial tissue is probably an important condition for the ultimate step of myometrial stimulation and the onset of labor.