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Adrenergic Stimulation of Placental Progesterone Production^*

Department of Obstetrics and Gynecology (S.N.C.) and the Division of Reproductive Biology (A.J.Z.), University of Pittsburgh School of Medicine, Magee-Womens Hospital, and the Department of Community Medicine (R.P.H.), University of Pittsburgh, Pittsburgh, Pennsylvania 15213

Address requests for reprints to: Steve N. Caritis, M.D., Magee- Womens Hospital, Forbes and Halket Street, Pittsburgh, Pennsylvania 15213.

Cells from term human placentas were maintained in culture, and progesterone production was monitored over 24 h. The β₁-adrenergic receptor agonist dobutamine (10^–5 M) and the β₂-adrenergic receptor agonist terbutaline (10^–5 M) increased progesterone production by 36 ± 19% and 49 ± 8% (±SE), respectively, compared with that in controls (P < 0.001). Propranolol (10^–5 M) completely blocked the stimulatory effects of both drugs. The cAMP analog 8-bromo-cAMP (0.5 mM) also significantly altered (increased) progesterone production compared with controls (P < 0.001), but this effect was not blocked to a significant degree by propranolol.

The -adrenergic receptor agonist methoxamine (10^–4-10^–6 M) did not significantly alter placental progesterone production compared with controls, and the stimulatory effect of terbutaline on progesterone production was not significantly affected by blockade of the -adrenergic receptor with phentolamine.

These data indicate that placental progesterone production can be significantly modulated by stimulation of β-adrenergic, but not by -adrenergic, receptors. This response may be mediated by increased intracellular cAMP. These findings may be important in considering other metabolic functions of the placenta as well as the treatment of preterm labor. (J Clin Endocrinol Metab 56: 969, 1983)

^* This work was supported by a grant from the Magee-Women's Hospital Research Fund.

Received July 12, 1982.

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