Using the technique of delayed implantation of blastocysts in the rat, hyperthyroidism counteracts the effects of progesterone deficiency upon blastocyst survival and implantation while hypothyroidism contributes to the severity of the progesterone deficiency. In non-pregnant rats, treated in a manner to duplicate the delayed implantation experiments, the localization pattern of alkaline phosphatase within the uterine endometrium closely corresponds with the fate of the blastocysts. Hyperthyroidism during progesterone deficiency restores to normal the distribution of uterine alkaline phosphatase while hypothyroidism is associated with a further depletion of uterine alkaline phosphatase. Oxygen consumption studies indicate that the changes in the alkaline phosphatase are not associated with changes in the general uterine metabolism.