51. Dose-related action of gonadotropin-releasing hormone on basal prostanoid production from the human term placenta.
- Author
-
Kang IS, Koong MK, Forman J, and Siler-Khodr TM
- Subjects
- Dinoprost biosynthesis, Dose-Response Relationship, Drug, Humans, 6-Ketoprostaglandin F1 alpha biosynthesis, Dinoprost analogs & derivatives, Gonadotropin-Releasing Hormone pharmacology, Placenta metabolism, Prostaglandins E biosynthesis, Prostaglandins F biosynthesis, Thromboxane B2 biosynthesis
- Abstract
The dose-related effect of gonadotropin-releasing hormone on placental prostanoids was studied with a perifusion system. Villous tissues were perifused with medium 199 (1 ml/hr) and at the beginning of the fifth hour, either 0, 10(-10), 10(-9), 10(-8), 10(-7), or 10(-6) mol/L gonadotropin-releasing hormone was added to the medium of triplicate chambers. The concentration of prostaglandin E, prostaglandin F, 13,14-dihydro-15-keto-prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha, and thromboxane B2 in the effluent medium, collected every hour, was determined by specific radioimmunoassay. The cumulative release after gonadotropin-releasing hormone treatment for each chamber was calculated, and replicate chambers were averaged. Linear regression analysis of the average for each dose from three different placentas was used to determine the dose-response relationship. Gonadotropin-releasing hormone significantly inhibited the release of placental prostaglandin E, prostaglandin F, and thromboxane B2 in a dose-dependent fashion. Gonadotropin-releasing hormone had no significant effect on 13,14-dihydro-15-keto-prostaglandin F2 alpha and 6-keto-prostaglandin F1 alpha, although there was an apparent increase in 13,14-dihydro-15-keto-prostaglandin F2 alpha. These data support the hypothesis that chorionic gonadotropin-releasing hormone inhibits prostanoid production from the placenta, which in turn may regulate various functions of prostanoids during pregnancy.
- Published
- 1991
- Full Text
- View/download PDF