Mechanisms for the emergence of catecholamine‐sensitive adenylate cyclase and β‐adrenergic receptors in cultured hepatocytes

FEBS Letters

Christoffersen, T.¹  Sandnes, D.¹  Sand, T.E.¹  Refsnes, M.¹  Jacobsen, S.¹  Melien, Ø.¹ 

[1] Department of Pharmacology, University of Oslo, PO Box 1057, Blindern, Oslo 3, Norway

关键词: β-Adrenergic receptor;    Adenylate cyclase;    Actinomycin D;    Cycloheximide;    Rat hepatocyte;    Primary culture;    MIX;    methylisobutylxanthine;    ICYP;    iodocyanopindolol;    CHX;    cycloheximide;    Act. D;    actinomycin D;   

DOI  :  10.1016/0014-5793(83)80304-4

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Adult male rat hepatocytes, which normally respond poorly to β-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 β-adrenoceptor ligand [¹²⁵I]cyanopindolol. The emergence of β-adrenergic responsiveness did not require cell attachment or serum. Addition of dexamethasone, insulin, thyroxine or dihydortestosterone to the cultures, singly or in combination, did not prevent the augmented β-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 β-adrenoceptor binding.

【 授权许可】

Unknown