It has been well known that estrogens stimulate the uterine contractility and progestins inhibit it. Then, one may expect that the uterine contractility and sensitivities to oxytocin (OT) and prostaglandin F_2α (PGF_2α) would be different among the estrus cycle. These hypotheses were tested using the mature female rat. Spontaneous isometric contractions of isolated uterine strips (1 X 0.3 cm) from cyclic rats in various stages of the estrus cycle, bilateral ovarectomized rats and hypophysectomized rats were recorded in absence or presence with estradiol-17β(E₂), progesterone (P₄), OT and PGF_2α. The results were summarized as follows: 1) The spontaneous uterine contractile force was the highest in the estrus rat and the lowest in the ovarectomized or the hypophysectomized rat. In the proestrus rat, the contractile frequency was the lowest (2.7 beats/10 min) and the contractile duration was the longest (70 sec). In the other groups, there were no any differencies in frequency (9 beats/10 min) and in duration (30 sec). 2) OT and PGF_2α stimulated the uterine contractility in all groups tested except in the hypophysectomized rat in which OT failed to stimulate the uterine contraction. PGF_2α was more effective in stimulating the uterine contraction than OT in all groups tested except in the estrus rat. OT-induced contraction was the highest in the estrus rat and PGF_2α-induced contraction was the lowest in the hypophysectomized rat. 3) Uterine contractilities were not changed by the in vitro treatments of E₂ or P₄ under the influence of endogenous steroids, however, E₂ and P₄ stimulated the uterine contraction in the ovarectomized rat in which endogenous steroids were almost abolished. 4) Increased uterine contraction by the treatment of OT was subpressed by in vitro E₂ or P₄ in the estrus rat, while it was potentiated by the P₄ in the proestrus rat. In other groups, exogenous E₂ or P₄ did not affect the OT-induced uterine contraction. 5) PGF_2α-induced uterine contraction was subpressed in the ovarectomized rat by E₂ and P₄, in the diestrus and proestrus rats by P₄ and in the hypophysectomized rat by E₂. In other groups, exogenous E₂ or P₄ was ineffective in altering the PGF_2α-induced uterine contraction. According to the above results, it may conclude that the mechanisms of the different uterine contractility and the different uterine sensitivity to OT or PGF_2α according to the estrus cycle are not explicable with only the serum concentrations of steroids, OT and PGF_2α but also other unknown factors.