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Corpus luteum function during the early postpartum interval in lactating rhesus monkeys: In vivo and in vitro response to exogenous gonadotropin

  • Richard L. Stouffer
  • , Laura A. Bennett
  • , Wilbert E. Nixon
  • , Gary D. Hodgen

Research output: Contribution to journalArticlepeer-review

Abstract

The response of the postpartum corpus luteum to exogenous gonadotropin was studied in 12 lactating rhesus monkeys given daily injections of either human chorionic gonadotropin (HCG, n = 6) or saline (control, n = 6) for 4 days immediately following parturition. Peripheral blood samples were collected daily. On the 5th day postpartum, luteectomy was performed and progesterone production by dispersed luteal cells was examined. Whereas progesterone in the peripheral circulation of control monkeys progressively declined between days 1 and 5 postpartum, progesterone levels increased significantly (p<0.025) with the onset of HCG treatment and remained significantly (p<0.025) elevated above the controls throughout the period of HCG treatment. However, despite the daily administration of HCG, circulating progesterone levels declined (p<0.05) between days 3 and 5 postpartum. The weight of the corpus luteum excised from HCG-treated macaques was significantly (p<0.005) greater than that of the controls. Dispersed cells from corpora lutea of saline-treated monkeys produced progesterone in vitro under control conditions (nutrient medium alone) and responded to the addition of high (100 ng/ml), but not low (1 ng/ml), levels of HCG with increased steroidogenesis. Although luteal cells from HCG-treated macaques tended to produce more progesterone in vitro than cells from control monkeys, they also exhibited a 50-fold reduction in sensitivity to HCG in vitro. These data suggest that the corpus luteum of lactating postpartum rhesus monkeys exhibited steroidogenic function which was stimulated by exogenous gonadotropin. However, prolonged exposure of the corpus luteum to high levels of exogenous gonadotropin appeared to produce a state of refractoriness to additional gonadotropic stimuli.

Original languageEnglish (US)
Pages (from-to)73-82
Number of pages10
JournalSteroids
Volume29
Issue number1
DOIs
StatePublished - Jan 1977
Externally publishedYes

Funding

Richard L. Stouffer, Laura A. Bennett*, Wilbert E. Nixon, and Gary D. Hodgen Section on Endocrinology, Reproduction Research Branch, National Institute of Child Health and Human Development, Auburn Building, Room 203, National Institutes of Health, Bethesda, Md. 20014, and *Office of Pesticide Programs, Environmental Protection Agency, Arlington, Va. 22202.

FundersFunder number
Auburn Building
Author National Institutes of Health National Institutes of Health National Institutes of Health National Institutes of Health The Bev Hartig Huntington's Disease Foundation National Institutes of Health20014
The National Institute of Child Health and Human Development
U.S. Environmental Protection Agency22202

    ASJC Scopus subject areas

    • Biochemistry
    • Molecular Biology
    • Endocrinology
    • Pharmacology
    • Clinical Biochemistry
    • Organic Chemistry

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