title: Effects of prostaglandin E and F receptor agonists in vivo on luteal function in ewes.
abstract: Loss of progesterone secretion at the end of the estrous cycle is via uterine PGF(2alpha) secretion; however, uterine PGF(2alpha) is not decreased during early pregnancy in ewes to prevent luteolysis. Instead the embryo imparts resistance to PGF(2alpha)-induced luteolysis, which is via the 2-fold increase in prostaglandins E(1) and E(2) (PGE(1), PGE(2); PGE) in the endometrium during early pregnancy. Chronic intrauterine infusion of PGE(1) or PGE(2) prevents spontaneous or an estradiol-17beta, IUD, or PGF(2alpha)-induced luteolysis. Four PGE receptor subtypes (EP(1), EP(2), EP(3), and EP(4)) and an FP receptor specific for PGF(2alpha) have been identified. The objective of this experiment was to determine the effects of EP(1), EP(2), EP(3), or FP receptor agonists in vivo on luteal mRNA for LH receptors, occupied and unoccupied LH receptors, and circulating progesterone in ewes. Ewes received a single treatment of 17-phenyl-tri-Nor-PGE(2) (EP(1), EP(3)), butaprost (EP(2)), 19-(R)-OH-PGE(2) (EP(2)), sulprostone (EP(1), EP(3)), or PGF(2alpha) (FP) receptor agonists into the interstitial tissue of the ovarian vascular pedicle adjacent to the luteal-containing ovary. 17-Phenlyl-tri-Nor-PGE(2) had no effect (P> or =0.05) on any parameter analyzed. Butaprost and 19-(R)-OH-PGE(2) increased (P< or =0.05) mRNA for LH receptors, occupied and unoccupied LH receptors, and circulating progesterone. Both sulprostone and PGF(2alpha) decreased (P< or =0.05) mRNA for LH receptors, occupied and unoccupied LH receptors, and circulating progesterone. It is concluded that both EP(3) and FP receptors may be involved in luteolysis. In addition, EP(2) receptors may mediate prevention of luteolysis via regulation of luteal mRNA for LH receptors to prevent loss of occupied and unoccupied LH receptors and therefore to sustaining luteal function.
authors.affiliation: Department of HNFAS, University of Hawaii, 1955 East-West Road, Honolulu, HI 96822, USA. weems@hawaii.edu
authors.forename: Y S
authors.initials: YS
authors.lastname: Weems
authors.forename: T M
authors.initials: TM
authors.lastname: Nett
authors.forename: L A
authors.initials: LA
authors.lastname: Rispoli
authors.forename: T L
authors.initials: TL
authors.lastname: Davis
authors.forename: D L
authors.initials: DL
authors.lastname: Johnson
authors.forename: T
authors.initials: T
authors.lastname: Uchima
authors.forename: A
authors.initials: A
authors.lastname: Raney
authors.forename: E
authors.initials: E
authors.lastname: Lennon
authors.forename: T
authors.initials: T
authors.lastname: Harbert
authors.forename: G
authors.initials: G
authors.lastname: Bowers
authors.forename: N
authors.initials: N
authors.lastname: Tsutahara
authors.forename: R D
authors.initials: RD
authors.lastname: Randel
authors.forename: C W
authors.initials: CW
authors.lastname: Weems
mesh_terms: D000818:Animals; D003338:Corpus Luteum / Q000033:anatomy & histology / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology*; D030762:Estrous Cycle / Q000187:drug effects / Q000378:metabolism; D005260:Female; D008184:Luteal Cells / Q000187:drug effects / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D011247:Pregnancy; D011374:Progesterone / Q000097:blood; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011974:Receptors, LH / Q000235:genetics; D011982:Receptors, Prostaglandin / Q000819:agonists*; D018078:Receptors, Prostaglandin E / Q000819:agonists*; D012756:Sheep
chemical_list: D012333:RNA, Messenger; D011974:Receptors, LH; D011982:Receptors, Prostaglandin; D018078:Receptors, Prostaglandin E; C034671:prostaglandin F2alpha receptor; D011374:Progesterone