Molecular Mechanisms Regulating Contractility of the Pregnant Uterus

Abstract

The changes in uterine contractility that take place several days or hours before birth, depending upon the species, are amongst the most dramatic seen in mammalian physiology [1,2]. The shift from the innervated nonpregnant uterus dominated by the effects of neurotransmitters, neuropeptides and sex steroids to the pregnant uterus potentially dominated by circulating factors, such as the sex steroids and locally produced agents from submyometrial tissues, is a particularly striking change [3–6]. This has been variously hypothesized as the explanation for the control of uterine contraction during labour residing with the fetus and intrauterine tissues and removed from the mother [7,8]. However, the reappearance of oxytocin, both circulating and of endometrial origin, as a potentially important stimulating of myometrial contraction, directly and indirectly, during labour implies that some maternal influence may be present in the later stages of birth [9]. Despite some evidence to the contrary, the labour-related production of prostaglandins, whether oxytocin stimulated or not, still appears to be the primary mechanism for initiating and sustaining uterine contraction through labour [10].