The Influence of Luteinizing Hormone (LH), Prolactin, and the Uterus on the Development of a Dependency on LH in the Control of Progesterone Secretion in the Pseudopregnant Rat1

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Abstract
LH-dependency in pseudopregnant (PSP) rats was determined by the luteolytic response (fall in serum progesterone, shortening of the diestrus duration and failure of decidual tissue (DT) formation) in response to treatment with an antiserum to LH (LHAS). PSP rats hypophysectomized and pituitary autotransplanted on day (d) 2 had no luteolytic response to LHAS treatment on either d 8, 9 or 10, while intact PSP rats, bearing a single pituitary homotransplant from d 2 on, had a pronounced response. The pituitary autotransplant-bearing rats had markedly lower serum LH levels than did intact rats; serum prolactin (PRL) was about 60 ng/ml in both autotransplant- and homotransplant-bearing rats. Treatment of the pituitary autotransplant-bearing rat with up to 20 .mu.g ovine LH/d from d 2-8 did not induce LH-dependency. Daily treatment of DT-bearing PSP rats (which normally become LH dependent by d 9), however, with LHAS from d 2-11, or from d 2-5 and again on d 9 did not cause any significant change in progesterone secretion, but when such rats were given LHAS on d 9 only, or only from d 5-11, progesterone secretion was drastically and permanently reduced. The effect of 1, 2 or 4 pituitary homotransplants/rat from d 2 on, in either DT-bearing or d 5 hysterectomized PSP rats, on the effect of LHAS treatment on d 9 was then studied. Among the hysterectomized rats, as little as 1 pituitary homotransplant prevented any luteolytic effect of LHAS. Among the DT-bearing rats, the homotransplants reduced the luteolytic effect of LHAS in proportion to their number, but even with 4 pituitary homotransplants/rat, the response was not reduced as much as in the hysterectomized rats. In both types of PSP rat, the homotransplants caused a dose-related increase in serum PRL and LH, and raised the serum progesterone level, after d 5, but without relation to the number of transplants. LH seems to induce LH-dependency when it is above a critical level during some part of the first week after ovulation. PRL seems to oppose this effect, and its effect is, in turn, opposed by the progestational uterus. The failure of LH treatment to induce LH dependency in the pituitary autotransplant-bearing rat could have been due to both the high level of prolactin and the absence of a progestationally active uterus in these rats.