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Endocrinology, doi:10.1210/endo-115-3-969
Endocrinology Vol. 115, No. 3 969-976
Copyright © 1984 by the Endocrine Society.
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Differential Action and Secretion of Rat Placental Lactogens*

LINDA A. GLASER{dagger}, PAUL A. KELLY{ddagger} and GEULA GIBORI

Department of Physiology and Biophysics, University of Illinois at Chicago College of Medicine, Health Sciences Center Chicago, Illinois 60612
The Laboratoire d’Endocrinohgie Moleculaire, Centre Hospitalier de I’Uniuersite Laval Quebec, G1V4G2, Canada

Address requests for reprints to: Dr. Geula Gibori, Department of Physiology and Biophysics, University of Illinois College of Medicine, Health Sciences Center, P.O. Box 6998, Chicago, Illinois 60680.

Abstract

The abilities of the two different mol wt forms of rat placental lactogen (rPL) to maintain luteal steroidogenesis in pregnant rats in the absence of PRL were determined. The two forms of rPL present in day 12 pregnant rat serum were separated by gel chromatography, lyophilized, and reconstituted in a volume of saline equal to the original volume of serum. Rats were injected with 0.4 mg ergocryptine (ECO) on day 6 of pregnancy to suppress PRL and were then treated with a preparation of the large mol wt (LMW) hormone, the small mol wt (SMW) hormone, or both molecules (2 ml/day). Control animals received saline. Twice daily injections of the amount of LMW hormone contained in 1 ml day 12 pregnant rat serum reversed the abortifacient effect of ECO. In contrast, administration of the SMW hormone did not maintain either pregnancy or progesterone levels. Administration of both mol wt forms of rPL was also capable of maintaining luteal function. Sera obtained from day 18 pregnant rats containing only the SMW hormone had no luteotropic activity when administered, yet treatment with sera of day 12 pregnant rats sustained progesterone synthesis and fetal survival after ECO treatment.

rPL were measured in the peripheral circulation and in the uterine vein throughout pregnancy by radioreceptor assay (RRA) using particulate membranes from either rabbit mammary gland or rat ovaries. Two peaks of activity were observed in the peripheral circulation by the two RRAs: one between days 11–14 and another between days 17–21, with a decline in activity between days 14–16. In contrast, levels of rPL in the uterine vein remained elevated throughout pregnancy. Concentrations of the LMW placental luteotropin were 5–10 times higher by ovarian RRA (O-RRA) than by mammary gland RRA (MGRRA) between days 11–13, but concentrations of the SMW placental lactogen were found by the two RRAs to be similar in the later stages of pregnancy. Gel filtration of day 12 pregnant rat serum revealed two peaks of PRL-like activity. The O-RRA detected 19 times more LMW placental luteotropin than did the MG-RRA in the first peak of activity, yet measured equivalent amounts of the SMW placental lactogen in the second peak. Similar to results found in the peripheral circulation, levels of LMW placental luteotropin in the uterine vein measured by MG-RRA were significantly lower than those determined by O-RRA until day 14 of pregnancy. During late pregnancy, however, both assays detected the same amount of PL in the uterine vein. Results of this investigation indicate that only the LMW placental luteotropin found at midpregnancy has luteotropic properties and that this placental luteotropin binds more effectively to the PRL receptor of the rat ovary than to the PRL receptor of the rabbit mammary gland. The results further suggest that the decline in peripheral levels of PLs between days 14–16 is not due to a decrease in secretion, but, rather, to a change in the MCR. (Endocrinology 115: 969–976, 1984)

Footnotes

* This work was supported by NIH Grants HD-11119 and HD-12356 and was presented in part at the 64th Annual Meeting of the Endocrine Society, San Francisco, CA, 1982.

{dagger} Submitted in partial fulfillment of the requirements for the Doctor of Philosophy degree in the Department of Physiology and Biophysics in the Graduate College at the University of Illinois at Chicago, Health Sciences Center.

{ddagger} Present address: Laboratory of Molecular Endocrinology, Royal Victoria Hospital, McGill University, Montreal, Quebec, H3A 1A1, Canada.

Received April 11, 1983.




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