A Role for Intraluteal Estrogen in the Mediation of Luteinizing Hormone Action on the Rat Corpus Luteum during Pregnancy*

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Abstract
The ability of rat corpora lutea to accumulate estradiol via aromatization of testosterone suggests that estradiol might have a direct role in the regulation of luteal function. Rats were treated with LH [luteinizing hormone] antiserum on day 10 of pregnancy or with LH antiserum plus testoserone which was administered by a testosterone-filled Silastic capsule implanted s.c. on day 9 and left in place until the end of the experiment on day 14. In rats treated with LH antiserum alone, serum progesterone, luteal estradiol content, and luteal cell nuclear content of estradiol receptor had decreased sharply within 24 h. whereas luteal LH receptor remained elevated. Treatment with LH antiserum plus a large testosterone implant prevented the decline in serum progesterone and nuclear estradiol receptor and caused a dramatic elevation in luteal estradiol content. By day 14, rats treated with antiserum alone had aborted, LH receptor content was reduced 92%, serum progesterone was 7 .+-. 1 ng/ml. luteal estradiol concentration was 15 .+-. 7 pg/mg tissue, and luteal growth had ceased. By contrast, in rats treated with HL antiserum plus the large testosterone capsule, LH receptor content was high, serum progesterone was 102 .+-. 8 ng/ml, luteal estradiol concentration was 82 .+-. 13 pg/mg tissue, and luteal growth was maintained. Estradiol concentration in luteal tissue of control pregnant rats on day 14 was 9.3 .+-. 0.5 pg/mg. To determine if this luteotropic effect of testosterone could be obtained with nonaromatizable androgen and if pharmacological concentrations of intraluteal estradiol were necessary for the maintenance of luteal function in the absence of LH, rats were treated with dihydrotestosterone (via a large Silastic capsule) or with low levels of testosterone by means of a small testosterone implant. When combined with LH antiserum treatment, dihydrotestosterone did not maintain luteal weight or serum progesterone. The small testosterone implant partillay maintained serum progesterone on day 14 (56 .+-. 10 ng ml), and maintained luteal estradiol at physiological concentrations (10 .+-. 1 pg/mg) luteal weight, and also pregnancy. Similar results were obtained in pregnant rats hypophysectomized on day 10 and treated with the small testosterone capsule. These results suggest that the luteotropic effect of LH is in reality a luteotropic action of estradiol which is formed within the corpora lutea from androgen.