||Regulation of Postnatal beta-Adrenergic Receptor/Adenylate Cyclase Development by Prenatal Agonist Stimulation and Steroids: Alterations in Rat Kidney and Lung after Exposure to Terbutaline or Dexamethasone.
Kudlacz, E. M. ;
Navarro, H. A. ;
Kavlock, R. J. ;
Slotkin, T. A. ;
||Duke Univ. Medical Center, Durham, NC. Dept. of Pharmacology.;Health Effects Research Lab., Research Triangle Park, NC. Developmental Toxicology Div.;Public Health Service, Rockville, MD.
||EPA-R-813769 ;PHS-HD-09713; EPA/600/J-90/526;
Beta adrenergic receptors ;
Adenylate cyclase ;
Prenatal exposure delayed effects ;
Body weight ;
Binding sites ;
||Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy.
Glucocorticoids and adrenergic stimulation are both thought to control the development of beta-adrenergic receptors/responses. In the current study, rats were exposed to dexamethasone or terbutaline during late gestation and the development of beta-binding capabilities and adenylate cyclase activity evaluated in membrane preparations from kidney and lung. Prenatal dexamethasone exposure produced postnatal adrenergic hyperreactivity of kidney adenylate cyclase; the effect resulted from increases in the enzyme itself, as both basal adenylate cyclase and forskolin-stimulation of the enzyme were also increased by dexamethasone. Similarly, prenatal terbutaline exposure evoked increases in basal, isoproterenol-stimulated and forskolin-stimulated adenylate cyclase in the kidney. In the lung, dexamethasone produced an initial postnatal deficit in basal asenylate cyclase and deficient responsiveness to isoproterenol, but the deficit resolved shortly after birth. Terbutaline selectively promoted the ability of isoproterenol to stimulate lung adenylate cyclase in the first few days after birth, without alterations in basal adenylate cyclase; this was followed by a period of prolonged subsensitivity of both basal and isoproterenol-stimulated activity.