The uterotrophic, anti-uterotrophic and contraceptive properties of several antifertility agents vere compared in female rats and hamsters. The compounds fell into two distinct groups on the basis of their biological profile in rats: 1. Estrogenic contraceptives, including estradiol-17β (E 2 ), 17α-ethynylestradiol (EE), diethylstilbestrol (DES), ORF 3858 and F 6066; 2. Anti-estrogenic contraceptives, including CN55,945-27, U11,555A, Su 13320 and MER-25. These classifications did not hold true for hamsters. E 2 and DES were only 4–5% as active in hamsters as in rats as uterotrophic or contraceptive agents; other estrogens were even less effective. For example, hamsters required 400 to 700 times more ORF 3858 than did rats for uterotrophic and contraceptive activity. Furthermore, enormous doses of all but one of the “anti-estrogenic” compounds failed to antagonize the uterotrophic action of E 2 or to impair fertility in hamsters. The data suggest that fertility may be inhibited in rats by administration of estrogens in highly uterotrophic doses or by treatment with compounds which antagonize the endogenous estrogen required for implantation and maintenance of pregnancy. In contrast, hamsters are less sensitive than rats to the contraceptive effects of estrogens and appear to respond minimally to compounds which are anti-estrogenic in rats.
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Four monkeys (Macaca Fascicularis) were given daily injections of 12 μg estradiol for 3 days starting on day 18 or 19 of the menstrual cycle and from day 3 of the estradiol treatment they were given daily injections of 15 mg PGF 2α . On the 3rd, 4th or 5th day of the treatment with PGF 2α all of the monkeys showed menstrual bleeding. Thus in every case there was shortening of the luteal phase of the cycle. Injections of PGF 2α alone, for 5 days, did not have this effect. In the pregnant monkey, treatment with 15 mg PGF 2α for 5 days, did not terminate pregnancy, whereas only 3 injections of the same dose of PGF 2α caused abortion in another monkey pretreated with 12 μg estradiol for 3 days. It is postulated that: 1. Administration of estrogen may cause a block of gonadotrophin release by a negative feedback mechanism. 2. Estrogen may also cause the release of endogenous prostaglandins. 3. The corpus luteum due to lack of gonadotrophins may become more vulnerable to exogenously administered and possibly also to endogenously secreted prostaglandins. 4. Estrogen may act directly on the ovary and make the luteal cells more sensitive to prostaglandins, for example by causing changes in vascular permeability.