title: Effects of prostaglandins E2 and F2alpha (PGE2; PGF2alpha), trilostane, mifepristone, palmitic acid (PA), indomethacin (INDO), ethamoxytriphetol (MER-25), PGE2 + PA, or PGF2alpha + PA on PGE2, PGF2alpha, and progesterone secretion by bovine corpora lutea of mid-pregnancy in vitro.
abstract: The effects of PGE2, PGF2alpha, trilostane, RU-486, PA, INDO, MER-25, PGE2, or PGF2alpha + PA on secretion of progesterone, PGE2, or PGF2alpha by bovine corpora lutea (CL) of mid-pregnancy in vitro for 4 and 8 hr was examined. Secretion of PGE2 and PGF2alpha increased with time in culture (P < or = 0.05). PGE2 and PGE2 + PA increased (P < or = 0.05) secretion of progesterone at 4 and 8 h, progesterone secretion was increased (P < or = 0.05) at 4 h; but not at 8 h (P > or = 0.05) by trilostane, mifepristone, PGF2alpha and PGF2alpha + PA, and was decreased at 8 h by PGF2alpha and PGF2alpha + PA. Indomethacin decreased (P < or = 0.05) secretion of PGE2, PGF2alpha, and progesterone at 4 and 8 h. Trilostane, PA, PGF2alpha, RU-486 and PGF2alpha + PA increased (P < or = 0.05) PGE2 at 4 h only. Palmitic acid decreased (P < or = 0.05) PGF2alpha at 4 h, while trilostane, RU-486, or MER-25 did not affect (P < or = 0.05) PGE2 of PGF2alpha secretion. It is concluded that PGE2 of luteal tissue origin is the luteotropin at mid-pregnancy in cows. Also, it is suggested that PA may alter progesterone secretion by affecting the inter conversion of PGE2 and PGF2alpha.
authors.affiliation: Department of Human Nutrition, Food and Animal Science, University of Hawaii, Honolulu, Hawaii 96822, USA.
authors.forename: Y S
authors.initials: YS
authors.lastname: Weems
authors.forename: A W
authors.initials: AW
authors.lastname: Lewis
authors.forename: R D
authors.initials: RD
authors.lastname: Randel
authors.forename: C W
authors.initials: CW
authors.lastname: Weems
mesh_terms: D000021:Abortifacient Agents, Steroidal / Q000494:pharmacology; D000818:Animals; D002417:Cattle; D003338:Corpus Luteum / Q000187:drug effects* / Q000378:metabolism*; D013196:Dihydrotestosterone / Q000031:analogs & derivatives* / Q000494:pharmacology; D015237:Dinoprost / Q000378:metabolism / Q000494:pharmacology; D015232:Dinoprostone / Q000378:metabolism / Q000494:pharmacology*; D004357:Drug Synergism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004965:Estrogen Antagonists / Q000494:pharmacology; D004978:Ethamoxytriphetol / Q000494:pharmacology; D005260:Female; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D015735:Mifepristone / Q000494:pharmacology; D010120:Oxytocics / Q000378:metabolism / Q000494:pharmacology*; D019308:Palmitic Acid / Q000494:pharmacology; D011247:Pregnancy; D011374:Progesterone / Q000378:metabolism*; D015149:Tocolytic Agents / Q000494:pharmacology
chemical_list: D000021:Abortifacient Agents, Steroidal; D004791:Enzyme Inhibitors; D004965:Estrogen Antagonists; D010120:Oxytocics; D015149:Tocolytic Agents; D013196:Dihydrotestosterone; D019308:Palmitic Acid; D015735:Mifepristone; D011374:Progesterone; D004978:Ethamoxytriphetol; D015237:Dinoprost; D015232:Dinoprostone; C009954:trilostane; D007213:Indomethacin