title: Physiological involvement of placental endothelin-1 and prostaglandin F2alpha in uteroplacental circulatory disturbance in pregnant rats exposed to heat stress.
abstract: Several studies suggest that heat stress affects placental functions including uteroplacental circulation, subsequently leading to pregnancy failure and birth weight reduction. To clarify the involvement of endothelin and placental prostaglandin (PG) systems in the uteroplacental circulation during heat stress, we examined the effects of i.v. administration of the endothelin receptor antagonist bosentan and the cyclooxygenase inhibitor indomethacin on uteroplacental blood flow and on placental PGE2 and PGF2alpha levels and their 13,14-dyhydro-15-keto-metabolites (PGEM and PGFM, respectively) in heat-exposed or non-heat-exposed pregnant rats. The administration of bosentan or indomethacin did not change uteroplacental blood flow in non-heat-exposed pregnant rats. In contrast, heat reduced uteroplacental blood flow in pregnant rats, but the reduction was reversed by the administration of bosentan or indomethacin before heat exposure. Heat did not change placental PGE2 or PGEM levels, but in pregnant rats it increased placental PGF2alpha and PGFM levels, which were reversed by bosentan or indomethacin. Our results suggest that the activation of placental endothelin receptor and PGF2alpha systems are involved in the uteroplacental circulatory disturbances produced by heat. PGF2alpha systems activated by heat may be involved in the vasoconstricting effects of endothelin-A and -B receptors during heat exposure.
authors.affiliation: Department of Environmental Medicine, Kochi University School of Medicine, Japan. hiro-n@po.incl.ne.jp
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Nakamura
authors.forename: Ichiyo
authors.initials: I
authors.lastname: Matsuzaki
authors.forename: Kotaro
authors.initials: K
authors.lastname: Hatta
authors.forename: Keiki
authors.initials: K
authors.lastname: Ogino
mesh_terms: D000818:Animals; D001831:Body Temperature; D000077300:Bosentan; D003106:Colon / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D015237:Dinoprost / Q000031:analogs & derivatives* / Q000737:chemistry / Q000378:metabolism / Q000502:physiology*; D065128:Endothelin Receptor Antagonists; D019332:Endothelin-1 / Q000502:physiology*; D005260:Female; D018882:Heat Stress Disorders / Q000378:metabolism / Q000503:physiopathology*; D007213:Indomethacin / Q000494:pharmacology; D007275:Injections, Intravenous; D007564:Japan; D010920:Placenta / Q000098:blood supply / Q000737:chemistry / Q000502:physiology*; D021041:Placental Circulation / Q000187:drug effects* / Q000502:physiology; D011247:Pregnancy; D051381:Rats; D017208:Rats, Wistar; D017466:Receptors, Endothelin / Q000187:drug effects / Q000378:metabolism; D013449:Sulfonamides / Q000008:administration & dosage / Q000493:pharmacokinetics
chemical_list: D016861:Cyclooxygenase Inhibitors; D065128:Endothelin Receptor Antagonists; D019332:Endothelin-1; D017466:Receptors, Endothelin; D013449:Sulfonamides; C008228:15-keto-13,14-dihydroprostaglandin F2alpha; D015237:Dinoprost; D000077300:Bosentan; D007213:Indomethacin