To study the mechanism of the ovulation-inhibiting effect of chlormadinone acetate, different quantities of this progestogen were implanted into one or both ovaries of dioestrous female rats. Introduction of the subcutaneously effective dose into one ovary suppressed ovulation in both, but implantation of half of this quantity did not influence spontaneous ovulation. On the other hand, 1/100 of the subcutaneously effective dose, implanted into the medio-basal hypothalamus or the anterior pituitary of adult dioestrous female rats, and of prepubertal females simultaneously injected with oestradiol benzoate, inhibited spontaneous and oestrogen-induced ovulations respectively. In juvenile rats the main site of action was the median eminence—anterior pituitary region. Chlormadinone was then implanted into the anterior hypothalamus or the anterior pituitary of adult dioestrous rats, and the median eminence was electrically stimulated during the 'critical period' in pro-oestrus. Since implants in the adenohypophysis prevented ovulation whereas implants in the anterior hypothalamus did not, a hypophysial site of action is suggested. On the basis of these results and of former findings on the action of oestrogens in ovulation, a hypothesis involving a competitive antagonism between oestrogen and progestogen at the hypophysial level is advanced to explain the acute ovulatory effects of these steroids.
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