Abstract

Parturition is a process that is composed of five separate and distinct physiological components but which lead from one to the next and are, therefore, interdependent. As such, the regulation of myometrial contractility should not be examined in isolation but as part of this continuum. The initiation of labor begins with the biochemical events that result in the rupture of the fetal membranes, effacement of the cervix, and the switch from contractures to contractions. Because we have defined being in labor as the point at which contractions no longer revert to contractures, we suggest that labor is superimposed upon pregnancy in humans and nonhuman primates. There is no withdrawal or retreat from pregnancy, and no evidence exists that the concentrations or actions of progesterone diminish at term. Rather, the target tissues of labor are activated to perform their physiological functions, and these functions are initiated by stimulators. The best candidate for achieving activation is maternal estrogen, derived from fetal DHEAS, but major gaps in our knowledge of this process still exist. Prostaglandins are the most likely candidates as the stimulators of labor initiation, but close inspection of their precise roles also demands that clearer definition of their synthesis and actions be acquired. Coordination of and communication between the physiological events of labor motivates us to examine nontraditional mediators such as cytokines for their potential roles in the regulation of these events at normal term.

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