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The Roles of Ca²⁺ and Adenosine 3',5'-Monophosphate in the Regulation of Progesterone Production by Human Placental Tissue

Department of Obstetrics and Gynecology, Hospital Pharmacy, Nagoya University School of Medicine Nagoya, Japan

Address requests for reprints to: Dr. Masahide Kasugai, Department of Obstetrics and Gynecology, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466, Japan.

The effects of Ca²⁺ and cAMP on progesterone production by placental tissue were studied. Term placentas obtained from normal pregnant women were perfused with sterile saline to remove blood, and the minced trophoblastic tissue was incubated in vitro. The rate of progesterone secretion by the trophoblastic tissue was 47.5 ± 5.0 (±SE) ng/mg cell protein ·h (control) at 450 µg low density lipoprotein/mL. The rates of progesterone production and cAMP accumulation were accelerated 3.0- and 1.7-fold, respectively, by 10^–5 M terbutaline, and the terbutaline effect was blocked by the addition of 50 µM N-(6-aminohexyl)5-chloro-l-naphthalenesulfonamide (W-7) or 50 µM trifluoperazine. Whereas progesterone secretion by placental explants cultured in medium containing low density lipoprotein with 1 µM A23187 (calcium ionophore) reached a rate of 128.5 ± 8.5 ng/mg cell protein·h, incubation of placental explants with A23187 caused a highly significant, dose-related decrease in terbutaline-stimulated cAMP accumulation in the presence of 3-isobutyl-l-methylxanthine, a phosphodiesterase inhibitor. Inhibition by A23187 was Ca²⁺ dependent, since incubation in a Ca²⁺-free medium with EGTA blocked its effect. Intracellular Ca²⁺ is apparently necessary for placental progesterone production; enhancement of progesterone production by β-stimulation is mediated by intracellular Ca²⁺ and cAMP.

Received September 2, 1986.

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