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Mechanisms for the emergence of catecholamine‐sensitive adenylate cyclase and β‐adrenergic receptors in cultured hepatocytes
Author(s) -
Refsnes M.,
Sandnes D.,
Melien Ø.,
Sand T.E.,
Jacobsen S.,
Christoffersen T.
Publication year - 1983
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(83)80304-4
Subject(s) - cyclase , endocrinology , medicine , adenylate kinase , catecholamine , cycloheximide , receptor , adrenergic receptor , biology , beta 3 adrenergic receptor , adrenergic , chemistry , cell culture , genetics
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 [ 125 I]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 [ 125 I]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.