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Children's Hospital Research Foundation and the Newborn Division, Departments of Pediatrics and Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine Cincinnati, Ohio 45267
Address all correspondence and requests for reprints to: Dr. Jeffrey A. Whitsett, Department of Pediatrics, University of Cincinnati, College of Medicine, Room 6103, 231 Bethesda Avenue, Cincinnati, Ohio 45267.
β-Adrenergic receptor and β-adrenergic sensitive adenylate cyclase were demonstrated in membrane fractions of human placenta. Placental membranes from normal term pregnancies bound the β-adrenergic antagonist (–)[3H]dihydroalprenolol to a single saturable class of sites (Kd = 2.31 ± 0.23 nM; n = maximal capacity, 112±9 fmol/mg). Competition for binding was stereoselective for (–)isomers of propranolol, and β-adrenergic agonists displayed competition for the placental receptor in the order (–)isoproterenol > (–)epinephrine > (–)norepinephrine, typical of a β2 type receptor. β-Adrenergic receptor was present in placental tissue as early as 10 weeks gestational age, and binding capacity decreased slightly with advancing gestation. [3H]Dihydroalprenolol binding was coupled to epinephrine-stimulated adenylate cyclase activity throughout gestation. The subcellular distribution of both β-adrenergic receptors and epinephrine-stimulated adenylate cyclase suggest their localization primarily in nonbrush border membrane fractions, presumably from plasma membranes more closely related to the fetal rather than to the maternal circulation. Epinephrinesensitive adenylate cyclase was not present in purified brush border preparations which were directly exposed to maternal blood in the intervillous space.
* This work was supported by NIH Grants HL-00414 and HL-22136 and NICDH Grant 11725.
Received June 15, 1979.
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