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REGULATION OF POSTNATAL B-ADRENERGIC RECEPTOR/ADENYLATE CYCLASE DEVELOPMENT BY PRENATAL AGONIST STIMULATION AND STEROIDS: ALTERATIONS IN RAT KIDNEY AND LUNG AFTER EXPOSURE TO TERBUTALINE OR DEXAMETHASONE
Citation:
Kudlacz, E., H. Navarro, R. Kavlock, AND T. Slotkin. REGULATION OF POSTNATAL B-ADRENERGIC RECEPTOR/ADENYLATE CYCLASE DEVELOPMENT BY PRENATAL AGONIST STIMULATION AND STEROIDS: ALTERATIONS IN RAT KIDNEY AND LUNG AFTER EXPOSURE TO TERBUTALINE OR DEXAMETHASONE. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-90/526 (NTIS PB91213496), 1990.
Description:
Glucocorticoids and adrenergic stimulation are both thought to control the development of adrenergic receptors/responses. n the current study, rats were exposed to dexamethasone or terbutaline during late gestation and the development of B-binding capabilities and adenylate cyclase activity evaluated in membrane preparations from kidney and lung. renatal 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. imilarly, prenatal terbutaline exposure evoked increases in basal, isoproterenol stimulated and forskolin-stimulated adenylate cyclase in the kidney. n the lung, dexamethasone produced an Initial postnatal deficit in basal adenylate cyclase and deficient responsiveness to isoproterenol, but the deficit resolved shortly after birth. erbutaline 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. lthough dexamethasone and terbutaline also caused significant changes in development of receptor binding capabilities, in neither tissue could these effects account for thi direction or magnitude of the changes in adenylate cyclase reactivity. hus, glucocorticoids and B-agonists can participate in the programming of development of postsynaptic reactivity by exerting actions upon post-receptor coupling mechanisms.