Mechanisms for the emergence of catecholamine-sensitive adenylate cyclase and beta-adrenergic receptors in cultured hepatocytes. Dependence on protein and RNA synthesis and suppression by isoproterenol |
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Authors: | M Refsnes D Sandnes O Melien T E Sand S Jacobsen T Christoffersen |
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Affiliation: | Department of Pharmacology, University of Oslo, PO Box 1057, Blindern, Oslo 3, Norway |
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Abstract: | Adult male rat hepatocytes, which normally respond poorly to beta-adrenergic agents, acquire such responsiveness during primary monolayer culture. We here show that the rise in catecholamine-sensitive adenylate cyclase activity in hepatocytes in vitro is closely paralleled by an increase in the ability to bind the beta-adrenoceptor ligand [125I]cyanopindolol. The emergence of beta-adrenergic responsiveness did not require cell attachment or serum. Addition of dexamethasone, insulin, thyroxine or dihydrotestosterone to the cultures, singly or in combination, did not prevent the augmented beta-adrenergic responsiveness. The increase in catecholamine-sensitive adenylate cyclase activity and [125I]cyanopindolol binding could be blocked by cycloheximide or actinomycin D. Exposure of the cultures to isoproterenol at 3-hourly intervals led to a dose-dependent suppression of the rise in isoproterenol-responsive adenylate cyclase and prevented the increase in beta-adrenoceptor binding. |
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Keywords: | β-Adrenergic receptor Adenylate cyclase Actinomycin D Cycloheximide Rat hepatocyte Primary culture MIX methylisobutylxanthine ICYP iodocyanopindolol CHX cycloheximide Act. D actinomycin D |
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