Refsnes M, Sandnes D, Melien O, Sand T E, Jacobsen S, Christoffersen T
FEBS Lett. 1983 Dec 12;164(2):291-8. doi: 10.1016/0014-5793(83)80304-4.
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.
成年雄性大鼠肝细胞通常对β-肾上腺素能药物反应不佳，但在原代单层培养过程中会获得这种反应能力。我们在此表明，体外培养的肝细胞中儿茶酚胺敏感的腺苷酸环化酶活性的升高与结合β-肾上腺素能受体配体[125I]氰胍心安的能力增加密切平行。β-肾上腺素能反应性的出现不需要细胞附着或血清。单独或联合向培养物中添加地塞米松、胰岛素、甲状腺素或二氢睾酮，均不能阻止增强的β-肾上腺素能反应性。儿茶酚胺敏感的腺苷酸环化酶活性和[125I]氰胍心安结合的增加可被环己酰亚胺或放线菌素D阻断。每隔3小时将培养物暴露于异丙肾上腺素会导致异丙肾上腺素反应性腺苷酸环化酶升高的剂量依赖性抑制，并阻止β-肾上腺素能受体结合的增加。
