title: Interaction between uterine PGE and PGF2 alpha production and the nitridergic system during embryonic implantation in the rat.
abstract: Embryonic implantation is a complex process in which both maternal and embryonic signals are involved. In the present study, we evaluated changes in uterine prostaglandins production and nitric oxide synthase (NOS) activity during the course of early pregnancy and their interaction during implantation in rats. Uterine phospholipase A2 (PLA2) activity is increased on days 5 (day of ovoimplantation) and 6, compared to preimplantation days (3 and 4). This enhanced activity might be responsible for the observed increase in uterine PGE and PGF2 alpha production observed on day 5 of pregnancy, which induces endometrial vascular permeability and decidualization. When embryo access to the uterus is impaired, the increase of PG production is suppressed. During postimplantation, PGE levels return to preimplantation values, while PGF2 alpha decreased with respect to preimplantation values. Uterine NOS activity is also increased on day 4 and reaches a maximum on day 5, with a profile similar to PGE and PGF2 alpha. Dexamethasone administered in vivo decreased uterine NOS activity on day 4 of pregnancy but not on day 5, suggesting the presence of at least two types of NOS enzymes in the early days of pregnancy. A competitive inhibitor of NOS, L-NAME (600 and 1000 microM) induced a decrease in PGE and PGF2 alpha production in uterine tissue on day 5 of pregnancy. These results suggest the existence of a physiologically relevant nitridergic system which modulates prostaglandin production in the rat uterus during embryonic implantation.
authors.affiliation: Centro de Estudios Farmacológicos y Botánicos (CEFYBO). Buenos Aires, Argentina.
authors.forename: V
authors.initials: V
authors.lastname: Novaro
authors.forename: V
authors.initials: V
authors.lastname: Rettori
authors.forename: E T
authors.initials: ET
authors.lastname: González
authors.forename: A
authors.initials: A
authors.lastname: Jawerbaum
authors.forename: A
authors.initials: A
authors.lastname: Faletti
authors.forename: G
authors.initials: G
authors.lastname: Canteros
authors.forename: M A
authors.initials: MA
authors.lastname: de Gimeno
mesh_terms: D000287:Administration, Topical; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D015237:Dinoprost / Q000378:metabolism*; D015777:Eicosanoids / Q000096:biosynthesis; D010064:Embryo Implantation / Q000502:physiology*; D047108:Embryonic Development / Q000502:physiology; D005260:Female; D005938:Glucocorticoids; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D010741:Phospholipases A / Q000378:metabolism*; D054467:Phospholipases A2; D011247:Pregnancy; D011453:Prostaglandins / Q000096:biosynthesis; D011458:Prostaglandins E / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D014599:Uterus / Q000187:drug effects / Q000378:metabolism*
chemical_list: D000893:Anti-Inflammatory Agents; D015777:Eicosanoids; D005938:Glucocorticoids; D011453:Prostaglandins; D011458:Prostaglandins E; D009569:Nitric Oxide; D003907:Dexamethasone; D015237:Dinoprost; D019001:Nitric Oxide Synthase; D010741:Phospholipases A; D054467:Phospholipases A2; D019331:NG-Nitroarginine Methyl Ester