Simon G, Filep J, Zelles T
Department of Pathophysiology, Semmelweis University Medical School, Budapest, Hungary.
Life Sci. 1990;47(22):2021-5. doi: 10.1016/0024-3205(90)90436-u.
Alpha adrenergic agonists and antagonists as clonidine, guanfacine, yohimbine, phenylephrine and prazosin inhibited the [3H]-QNB binding to rat brain cortex muscarinic acetylcholine receptor (mAChR, M-1 subtype), heart (M-2 subtype) and parotid gland homogenate (M-3 subtype) in a dose-dependent competitive fashion. Ki values were between 10(-6) and 10(-3) M. Hill coefficients were about 1. No correlation was found between mAChR inhibiting capacity of these drugs and their activity on alpha adrenergic receptors. In contrast, other transmitters, as dopamine, GABA, glutamic acid, histamine, serotonin, isoproterenol and platelet activating factor (PAF) did not affect the QNB binding.
α-肾上腺素能激动剂和拮抗剂，如可乐定、胍法辛、育亨宾、去氧肾上腺素和哌唑嗪，以剂量依赖性竞争方式抑制[3H]-QNB与大鼠脑皮质毒蕈碱型乙酰胆碱受体（mAChR，M-1亚型）、心脏（M-2亚型）和腮腺匀浆（M-3亚型）的结合。Ki值在10(-6)至10(-3) M之间。希尔系数约为1。未发现这些药物的mAChR抑制能力与其对α-肾上腺素能受体的活性之间存在相关性。相比之下，其他递质，如多巴胺、γ-氨基丁酸、谷氨酸、组胺、5-羟色胺、异丙肾上腺素和血小板活化因子（PAF）不影响QNB结合。
