ラット腹水肝癌Adenylate Cyclaseのカテコラミンによる活性化とアドレナリン作働性β-受容体遮断薬によるその抑制

概要

論文の詳細を見る
Activation of adenylate cyclase of rat ascites hepatoma, AH-130,AH-272,AH-66,and AH-7974,by catecholamines, glucagon, and sodium fluoride, and effects of β-adrenergic blocking agents were studied. Basal adenylate cyclase activity of AH-7974 was higher than those of other three tumors as well as of the liver. Adenylate cyclase of AH-130 was activated by epinephrine and isoproterenol more than that of the liver, but those of other tumors showed lower responses to catecholamines. The response of tumor adenylate cyclase to glucagon was very low compared with that of the liver. Sodium fluoride activated all the tumor adenylate cyclases tested. The activation of AH-130 adenylate cyclase by epinephrine was inhibited by β-adrenergic blocking agents such as bufetolol, practolol, propranolol, and alprenolol, but was not blocked by α-adrenergic blocking agents like phentolamine and phenoxybenzamine, and by antitumor alkylating agents, bis(3-methylsulfonyloxypropyl) amine p-toluene sulfonate and nitrogen mustard. The effect of practolol, a selective β_1-adrenergic blocking agent, was less than other three agents. These results suggest that AH-130 possesses β_2-adrenergic receptor coupled with adenylate cyclase and may be useful as a tissue in place of liver for research on β-adrenergic blocking agents.
公益社団法人日本薬学会の論文
1976-11-25