Intraluteal infusions of prostaglandins of the E, D, I, and A series prevent PGF(2α)-induced, but not spontaneous, luteal regression in rhesus monkeys

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    Abstract

    A luteotropic role for prostaglandins (PGs) during the luteal phase of the menstrual cycle of rhesus monkeys was suggested by the observation that intraluteal infusion of a PG synthesis inhibitor caused premature luteolysis. This study was designed to identify PGs that promote luteal function in primates. First, the effects of various PGs on progesterone (P) production by macaque luteal cells were examined in vitro. Collagenase-dispersed luteal cells from midluteal phase of the menstrual cycle (Day 6 - 7 after the estimated surge of LH, n = 3) were incubated with 0 - 5000 ng/ml PGE2, PGD2, 6βPGI1 (a stable analogue of PGI2), PGA2, or PGF(2α) alone or with hCG (100 ng/ml). PGE2, PGD2, and 6βPGI1 alone stimulated (p <0.05) P production to a similar extent (2- to 3-fold over basal) as hCG alone, whereas PGA2 and PGF(2α) alone had no effect on P production. Stimulation (p <0.05) of P synthesis by PGE2, PGF2, and 6βPGI1 in combination with hCG was similar to that of hCG alone. Whereas PGA2 inhibited gonadotropin-induced P production (p <0.05), that in the presence of PGF(2α) plus hCG tended (p =0.05) to remain elevated. Second, the effects of various PGs on P production during chronic infusion into the CL were studied in vivo. Saline with or without 0.1% BSA (n = 12), PGE2 (300 ng/h; n = 4), PGD2 (300 ng/h; n = 4), 6βPGI1 (500 ng/h; n = 3), PGA2 (300 ng/h, n = 4), or PGF(2α) (10 ng/h; n = 8) was infused via osmotic minipump beginning at midluteal phase (Days 5 - 8 after the estimated LH surge) until menses. In addition, the same dose of PGE, PGD, PGI, or PGA was infused in combination with PGF(2α) (n = 3 - 4/group) for 7 days. P levels over 5 days preceding treatment were not different among groups. In 5 of 8 monkeys receiving PGF(2α) alone, P declined to <0.5 ng/ml within 72 h after initiation of infusion and was lower (p <0.05) than controls. The length of the luteal phase in PGF(2α)-infused monkeys was shortened (12.3 ± 0.9 days; mean ± SEM, n = 8; p <0.05) compared to controls (15.8 ± 0.5). Intraluteal infusion of PGE, PGD, PGI, or PGA alone did not affect patterns of circulating P or luteal phase length. In contrast, intraluteal infusion of PGE, PGD, or PGA in combination with PGF(2α) maintained P levels during the infusion period and prevented the premature menses seen with infusion of PGF(2α) alone. Although P levels were consistently lower than controls during 3 days after initiation of 6βPGI1 plus PGF(2α) infusion, luteal phase length in these monkeys was similar to controls. Thus, PGs that stimulate steroidogenesis in vitro will prevent premature luteolysis induced by exogenous PGF(2α) was antigonadotropic in vitro, it did not suppress luteal function in vivo, but counteracted the luteolytic effect of exogenous PGF(2α).

    Original languageEnglish (US)
    Pages (from-to)507-516
    Number of pages10
    JournalBiology of Reproduction
    Volume43
    Issue number3
    DOIs
    StatePublished - 1990

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    Prostaglandins D
    Luteolysis
    Prostaglandins F
    Prostaglandins E
    Macaca mulatta
    Luteal Phase
    Prostaglandins
    Prostaglandins A
    Dinoprostone
    Prostaglandin D2
    Haplorhini
    Luteal Cells
    Menstruation
    Corpus Luteum
    Luteolytic Agents
    Prostaglandin Antagonists
    Dinoprost
    Macaca
    Collagenases
    Epoprostenol

    ASJC Scopus subject areas

    • Cell Biology
    • Developmental Biology
    • Embryology

    Cite this

    @article{5c543204ac6b48c58eb2751073811e39,
    title = "Intraluteal infusions of prostaglandins of the E, D, I, and A series prevent PGF(2α)-induced, but not spontaneous, luteal regression in rhesus monkeys",
    abstract = "A luteotropic role for prostaglandins (PGs) during the luteal phase of the menstrual cycle of rhesus monkeys was suggested by the observation that intraluteal infusion of a PG synthesis inhibitor caused premature luteolysis. This study was designed to identify PGs that promote luteal function in primates. First, the effects of various PGs on progesterone (P) production by macaque luteal cells were examined in vitro. Collagenase-dispersed luteal cells from midluteal phase of the menstrual cycle (Day 6 - 7 after the estimated surge of LH, n = 3) were incubated with 0 - 5000 ng/ml PGE2, PGD2, 6βPGI1 (a stable analogue of PGI2), PGA2, or PGF(2α) alone or with hCG (100 ng/ml). PGE2, PGD2, and 6βPGI1 alone stimulated (p <0.05) P production to a similar extent (2- to 3-fold over basal) as hCG alone, whereas PGA2 and PGF(2α) alone had no effect on P production. Stimulation (p <0.05) of P synthesis by PGE2, PGF2, and 6βPGI1 in combination with hCG was similar to that of hCG alone. Whereas PGA2 inhibited gonadotropin-induced P production (p <0.05), that in the presence of PGF(2α) plus hCG tended (p =0.05) to remain elevated. Second, the effects of various PGs on P production during chronic infusion into the CL were studied in vivo. Saline with or without 0.1{\%} BSA (n = 12), PGE2 (300 ng/h; n = 4), PGD2 (300 ng/h; n = 4), 6βPGI1 (500 ng/h; n = 3), PGA2 (300 ng/h, n = 4), or PGF(2α) (10 ng/h; n = 8) was infused via osmotic minipump beginning at midluteal phase (Days 5 - 8 after the estimated LH surge) until menses. In addition, the same dose of PGE, PGD, PGI, or PGA was infused in combination with PGF(2α) (n = 3 - 4/group) for 7 days. P levels over 5 days preceding treatment were not different among groups. In 5 of 8 monkeys receiving PGF(2α) alone, P declined to <0.5 ng/ml within 72 h after initiation of infusion and was lower (p <0.05) than controls. The length of the luteal phase in PGF(2α)-infused monkeys was shortened (12.3 ± 0.9 days; mean ± SEM, n = 8; p <0.05) compared to controls (15.8 ± 0.5). Intraluteal infusion of PGE, PGD, PGI, or PGA alone did not affect patterns of circulating P or luteal phase length. In contrast, intraluteal infusion of PGE, PGD, or PGA in combination with PGF(2α) maintained P levels during the infusion period and prevented the premature menses seen with infusion of PGF(2α) alone. Although P levels were consistently lower than controls during 3 days after initiation of 6βPGI1 plus PGF(2α) infusion, luteal phase length in these monkeys was similar to controls. Thus, PGs that stimulate steroidogenesis in vitro will prevent premature luteolysis induced by exogenous PGF(2α) was antigonadotropic in vitro, it did not suppress luteal function in vivo, but counteracted the luteolytic effect of exogenous PGF(2α).",
    author = "Mary Zelinski and Richard Stouffer",
    year = "1990",
    doi = "10.1095/biolreprod43.3.507",
    language = "English (US)",
    volume = "43",
    pages = "507--516",
    journal = "Biology of Reproduction",
    issn = "0006-3363",
    publisher = "Society for the Study of Reproduction",
    number = "3",

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    TY - JOUR

    T1 - Intraluteal infusions of prostaglandins of the E, D, I, and A series prevent PGF(2α)-induced, but not spontaneous, luteal regression in rhesus monkeys

    AU - Zelinski, Mary

    AU - Stouffer, Richard

    PY - 1990

    Y1 - 1990

    N2 - A luteotropic role for prostaglandins (PGs) during the luteal phase of the menstrual cycle of rhesus monkeys was suggested by the observation that intraluteal infusion of a PG synthesis inhibitor caused premature luteolysis. This study was designed to identify PGs that promote luteal function in primates. First, the effects of various PGs on progesterone (P) production by macaque luteal cells were examined in vitro. Collagenase-dispersed luteal cells from midluteal phase of the menstrual cycle (Day 6 - 7 after the estimated surge of LH, n = 3) were incubated with 0 - 5000 ng/ml PGE2, PGD2, 6βPGI1 (a stable analogue of PGI2), PGA2, or PGF(2α) alone or with hCG (100 ng/ml). PGE2, PGD2, and 6βPGI1 alone stimulated (p <0.05) P production to a similar extent (2- to 3-fold over basal) as hCG alone, whereas PGA2 and PGF(2α) alone had no effect on P production. Stimulation (p <0.05) of P synthesis by PGE2, PGF2, and 6βPGI1 in combination with hCG was similar to that of hCG alone. Whereas PGA2 inhibited gonadotropin-induced P production (p <0.05), that in the presence of PGF(2α) plus hCG tended (p =0.05) to remain elevated. Second, the effects of various PGs on P production during chronic infusion into the CL were studied in vivo. Saline with or without 0.1% BSA (n = 12), PGE2 (300 ng/h; n = 4), PGD2 (300 ng/h; n = 4), 6βPGI1 (500 ng/h; n = 3), PGA2 (300 ng/h, n = 4), or PGF(2α) (10 ng/h; n = 8) was infused via osmotic minipump beginning at midluteal phase (Days 5 - 8 after the estimated LH surge) until menses. In addition, the same dose of PGE, PGD, PGI, or PGA was infused in combination with PGF(2α) (n = 3 - 4/group) for 7 days. P levels over 5 days preceding treatment were not different among groups. In 5 of 8 monkeys receiving PGF(2α) alone, P declined to <0.5 ng/ml within 72 h after initiation of infusion and was lower (p <0.05) than controls. The length of the luteal phase in PGF(2α)-infused monkeys was shortened (12.3 ± 0.9 days; mean ± SEM, n = 8; p <0.05) compared to controls (15.8 ± 0.5). Intraluteal infusion of PGE, PGD, PGI, or PGA alone did not affect patterns of circulating P or luteal phase length. In contrast, intraluteal infusion of PGE, PGD, or PGA in combination with PGF(2α) maintained P levels during the infusion period and prevented the premature menses seen with infusion of PGF(2α) alone. Although P levels were consistently lower than controls during 3 days after initiation of 6βPGI1 plus PGF(2α) infusion, luteal phase length in these monkeys was similar to controls. Thus, PGs that stimulate steroidogenesis in vitro will prevent premature luteolysis induced by exogenous PGF(2α) was antigonadotropic in vitro, it did not suppress luteal function in vivo, but counteracted the luteolytic effect of exogenous PGF(2α).

    AB - A luteotropic role for prostaglandins (PGs) during the luteal phase of the menstrual cycle of rhesus monkeys was suggested by the observation that intraluteal infusion of a PG synthesis inhibitor caused premature luteolysis. This study was designed to identify PGs that promote luteal function in primates. First, the effects of various PGs on progesterone (P) production by macaque luteal cells were examined in vitro. Collagenase-dispersed luteal cells from midluteal phase of the menstrual cycle (Day 6 - 7 after the estimated surge of LH, n = 3) were incubated with 0 - 5000 ng/ml PGE2, PGD2, 6βPGI1 (a stable analogue of PGI2), PGA2, or PGF(2α) alone or with hCG (100 ng/ml). PGE2, PGD2, and 6βPGI1 alone stimulated (p <0.05) P production to a similar extent (2- to 3-fold over basal) as hCG alone, whereas PGA2 and PGF(2α) alone had no effect on P production. Stimulation (p <0.05) of P synthesis by PGE2, PGF2, and 6βPGI1 in combination with hCG was similar to that of hCG alone. Whereas PGA2 inhibited gonadotropin-induced P production (p <0.05), that in the presence of PGF(2α) plus hCG tended (p =0.05) to remain elevated. Second, the effects of various PGs on P production during chronic infusion into the CL were studied in vivo. Saline with or without 0.1% BSA (n = 12), PGE2 (300 ng/h; n = 4), PGD2 (300 ng/h; n = 4), 6βPGI1 (500 ng/h; n = 3), PGA2 (300 ng/h, n = 4), or PGF(2α) (10 ng/h; n = 8) was infused via osmotic minipump beginning at midluteal phase (Days 5 - 8 after the estimated LH surge) until menses. In addition, the same dose of PGE, PGD, PGI, or PGA was infused in combination with PGF(2α) (n = 3 - 4/group) for 7 days. P levels over 5 days preceding treatment were not different among groups. In 5 of 8 monkeys receiving PGF(2α) alone, P declined to <0.5 ng/ml within 72 h after initiation of infusion and was lower (p <0.05) than controls. The length of the luteal phase in PGF(2α)-infused monkeys was shortened (12.3 ± 0.9 days; mean ± SEM, n = 8; p <0.05) compared to controls (15.8 ± 0.5). Intraluteal infusion of PGE, PGD, PGI, or PGA alone did not affect patterns of circulating P or luteal phase length. In contrast, intraluteal infusion of PGE, PGD, or PGA in combination with PGF(2α) maintained P levels during the infusion period and prevented the premature menses seen with infusion of PGF(2α) alone. Although P levels were consistently lower than controls during 3 days after initiation of 6βPGI1 plus PGF(2α) infusion, luteal phase length in these monkeys was similar to controls. Thus, PGs that stimulate steroidogenesis in vitro will prevent premature luteolysis induced by exogenous PGF(2α) was antigonadotropic in vitro, it did not suppress luteal function in vivo, but counteracted the luteolytic effect of exogenous PGF(2α).

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