Abstract
β-Adrenergic stimulation of the placenta causes increased glycogenolysis and cAMP production. These effects are presumably mediated through the β-adrenergic receptor (βAR). In this study the βAR in rabbit placenta was characterized and shown to increase with gestational age. Binding of the β-adrenergic antagonist dihydroalprenolol, (-)[3H]DHA, to rabbit placental membranes was saturable to a single class of sites, KD=1.67±.07(nM), n=11 and Bmax=326±33 fmoles/mg. Agonist competition for the βAR was performed in the presence of the non-hydrolyzable GTP analog Gpp(NH)p (required for Hill coefficient = 1) and showed the potency order (-)iso ≫ (-)epi > (-)norepi characteristic of the β2 subtype. However, competition experiments with subtype specific agents metoprolol (β1) and zinterol (β2) indicated that the rabbit placenta contained approximately equal populations of βAR subtypes (51% β1, 49% β2). Rabbit placenta βAR/DNA increased 5.3 fold from day 16 to day 27 of gestation (410±120 fmoles/mg DNA to 2184±354 p<.001). During this interval protein/DNA (25±1.8mg/mg DNA to 34.2± 4.1) and DNA (4.0±.2mg/gm tissue to 3.5±.2) changed less markedly. KD did not change with gestation. (−)[3H]DHA binding was coupled with catecholamine stimulated adenylate cyclase (1.5 fold stimulation, p<.01). Rabbit placenta has two βAR (β1 and β2) in high density coupled to adenylate cyclase. Maximal βAR density occurs in late gestation coincident with the known catecholamine surge in fetal rodents suggesting a regulatory role for catecholamines in placental metabolism.
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Moore, J., Whitsett, J. 348 ONTOGENY OF THE β-ADRENERGIC RECEPTOR IN RABBIT PLACENTA. Pediatr Res 15 (Suppl 4), 498 (1981). https://doi.org/10.1203/00006450-198104001-00359
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DOI: https://doi.org/10.1203/00006450-198104001-00359