1964
DOI: 10.1530/acta.0.0460157
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Abstract: Based on absolute doses required to reach the defined end points in rats, it is proposed that inhibition of implantation or of ovulation per se cannot explain the efficacy of norethynodrel in inhibiting fecundity in female rats. The small size of the dose required to demonstrate gonadotrophin suppression indicates that this action, with consequent inhibition of follicular development, is the probable cause of the anti-fertility effect.

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Cited by 9 publications
(4 citation statements)
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“…Moreover, it was postulated that higher doses of these agents suppressed lh release and/or the ovarian response to lh. In another communication, Coppola & Perrine (1965b) reported that oral administration of the synthetic progestin, norethynodrel (40 mg/kg), caused a total blockade of ovulation in the PMS-treated immature rat. In agreement with Saunders (1964), it was suggested that this effect of norethynodrel was mediated through interference with lh release. Further support for this hypothesis was provided by the present investigation.…”
Section: Introductionsupporting
confidence: 65%
“…Moreover, it was postulated that higher doses of these agents suppressed lh release and/or the ovarian response to lh. In another communication, Coppola & Perrine (1965b) reported that oral administration of the synthetic progestin, norethynodrel (40 mg/kg), caused a total blockade of ovulation in the PMS-treated immature rat. In agreement with Saunders (1964), it was suggested that this effect of norethynodrel was mediated through interference with lh release. Further support for this hypothesis was provided by the present investigation.…”
Section: Introductionsupporting
confidence: 65%
“…Eckstein & Mandl (1962) and Harper (1964) reported experiments in which the induction of ovulation by exogenous gonadotrophins in intact rats was in some way facilitated by chlormadinone. From indirect evidence also, a number of workers have suggested that the antiovulatory steroids block ovulation by, in some way, inhibiting gonadotrophin release (Brennan & Kraay, 1963;Saunders, 1964). On the other hand, some evidence from clinical studies suggests that the antiovulatory steroids may depress ovarian sensitivity to the action of gonadotrophins (Lunenfeld, Sulimovici & Rabau, 1962;Brown et al 1962).…”
Section: Discussionmentioning
confidence: 99%
“…The former investigators believe that norethynodrel prevents fertilization of the ovum when it does not block ovulation. According to Saunders (1964), the primary con¬ traceptive action of norethynodrel is pre-ovulatory because the dose necessary to prevent nidation is much greater than the dose needed to prevent fertility when given during follicular development, although inhibition of ovulation as such cannot account for the anti-fertility effect.…”
Section: Discussionmentioning
confidence: 99%