title: Regulation of bovine oviductal NO synthesis by follicular steroids and prostaglandins.
abstract: Nitric oxide (NO) is a regulator of sperm motility, oocyte/embryo survival, and waves of contraction/relaxation in mammalian oviducts. As follicles control oviductal functions by two routes at least, (1) a systemic way via blood vessels before ovulation, (2) a direct way by entering of follicular fluid through fimbria at ovulation, we hypothesized that NO synthesis in the bovine oviduct is regulated by follicular steroids and prostaglandins (PGs). Quantification of mRNA expressions in the ampullary tissues showed that inducible NO synthase (NOS2) mRNA expression was highest on the day of ovulation (day 0). By contrast, NOS2 mRNA expression in the isthmus was highest on days 5-6 and lowest on days 19-21. Endothelial NOS (NOS3) mRNA expressions in either the ampulla or the isthmus did not change during the estrous cycle. PGE2 and PGF2α increased NOS2 mRNA expressions in cultured ampullary oviductal epithelial cells after 1-h incubation. These increases were suppressed by an antagonist of E-prostanoid receptor type 2, one of the PGE2 receptor. Estradiol-17β decreased the expression of NOS2 mRNA expression in cultured isthmic epithelial cells 24h after treatment. This effect was suppressed by an antagonist of estrogen receptorα(ESR1). Expression of ESR1 was highest on days 19-21 in the isthmic tissues. The overall findings indicate region-specific difference of NO synthesis in the oviduct. PGs flowed from ruptured follicle may up-regulate NO synthesis in the oviductal epithelium, whereas circulating E2 seems to inhibit NO synthesis via ESR1 in the isthmus at the follicular stage.
authors.affiliation: Laboratory of Reproductive PhysiologyGraduate School of Environmental and Life Science, Okayama University, Okayama, Japan.
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Kobayashi
authors.affiliation: Laboratory of Reproductive PhysiologyGraduate School of Environmental and Life Science, Okayama University, Okayama, Japan.
authors.forename: Yuki
authors.initials: Y
authors.lastname: Yamamoto
authors.affiliation: Animal Biotechnology GroupAnimal Research Center, Hokkaido Research Organization, Hokkaido, Japan.
authors.forename: Soichi
authors.initials: S
authors.lastname: Kageyama
authors.affiliation: Animal Biotechnology GroupAnimal Research Center, Hokkaido Research Organization, Hokkaido, Japan.
authors.forename: Hiroki
authors.initials: H
authors.lastname: Hirayama
authors.affiliation: Laboratory of Reproductive PhysiologyGraduate School of Environmental and Life Science, Okayama University, Okayama, Japan.
authors.forename: Koji
authors.initials: K
authors.lastname: Kimura
authors.affiliation: Laboratory of Reproductive PhysiologyGraduate School of Environmental and Life Science, Okayama University, Okayama, Japan Obihiro University of Agriculture and Veterinary MedicineHokkaido, Japan kokuda@okayama-u.ac.jp.
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Okuda
mesh_terms: D000818:Animals; D002417:Cattle; D002478:Cells, Cultured; D015237:Dinoprost / Q000378:metabolism; D004958:Estradiol / Q000494:pharmacology*; D030762:Estrous Cycle / Q000187:drug effects / Q000378:metabolism; D005187:Fallopian Tubes / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D009569:Nitric Oxide / Q000378:metabolism*; D006080:Ovarian Follicle / Q000187:drug effects / Q000378:metabolism*; D011453:Prostaglandins / Q000494:pharmacology*
chemical_list: D011453:Prostaglandins; D009569:Nitric Oxide; D004958:Estradiol; D015237:Dinoprost