The effects of the antiprogesterone compound RU 486 on preterm delivery, myometrial gap junctions, and plasma levels of steroid hormones were investigated in pregnant rats. Injection of RU 486 on day 16 of gestation resulted in prolonged delivery beginning after 24 hours. The preterm birth initiated by RU 486 was preceded and accompanied by the extensive development of gap junctions between myometrial cells. R 5020, but neither progesterone nor dexamethasone, prevented preterm birth and the development of gap junctions. Estrogen and progesterone levels declined after RU 486 treatment but only after a major proportion of the fetuses were delivered. This study indicates that progesterone may normally inhibit uterine contractility by suppressing the genome responsible for the expression of gap junctions.