Speeg K V, Wang S, Avant G R, Parker R, Schenker S
J Lab Clin Med. 1981 Jan;97(1):112-2.
Antihistamines directed at either the H1 or H2 histamine receptor have the well-known side effect of sedation. The mechanism for the CNS depressant action of antihistamines is unknown. We examine here the possibility that the mechanism may involve modulation of the cerebral benzodiazepine receptor. We demonstrate that cimetidine and pyrilamine are competitive antagonists of 3H-benzodiazepine binding to human cerebral receptor in vitro. The inhibition of radioligand binding was not specific for benzodiazepine receptor, however, since antihistamines also antagonized binding to GABA, opiate, and muscarinic acetylcholine receptor. The interaction of antihistamine with CNS receptors other than histamine receptor may explain, at least in part, the side effect of sedation.
作用于H1或H2组胺受体的抗组胺药具有众所周知的镇静副作用。抗组胺药产生中枢神经系统抑制作用的机制尚不清楚。我们在此研究该机制可能涉及对脑苯二氮䓬受体调节的可能性。我们证明,西咪替丁和吡拉明在体外是3H-苯二氮䓬与人脑受体结合的竞争性拮抗剂。然而,放射性配体结合的抑制并非苯二氮䓬受体所特有,因为抗组胺药也能拮抗与GABA、阿片和毒蕈碱型乙酰胆碱受体的结合。抗组胺药与组胺受体以外的中枢神经系统受体之间的相互作用可能至少部分解释了镇静副作用。