Rand M, Law M, Story D F, McCulloch M W
Drugs. 1976;11 SUPPL 1:134-43. doi: 10.2165/00003495-197600111-00029.
The peripheral actions of beta-adrenoreceptor antagonists on adrenergic transmitter mechanisms have been reviewed. In addition to receptor blockade, beta-adrenoreceptor antagonists may in high concentrations inhibit neuronal uptake of noradrenaline; inhibit monoamine oxidase; inhibit the uptake of noradrenaline into transmitter storage vesicles and inhibit the extraneuronal uptake of noradrenaline. High concentrations of beta-adrenoreceptor antagonists (threshold about 30 muM) also release noradrenaline from intraneuronal stores; however, their intrinsic sympathomimetic activity is generally attributed to their partial agonist property. Beta-adrenoreceptor antagonists possess adrenergic neurone blocking activity and quinidine-like or local anaesthetic activity. The existance of a positive feedback mechanism involving prejunctional beta-adrenoreceptors is discussed. It is suggested that bradycardia produced by beta-adrenoreceptor antagonists is due to blockade of the action of circulating catecholamines or of transmitter noradrenaline at cardiac extrajunctional beta-adrenoreceptor sites.
β-肾上腺素能受体拮抗剂对肾上腺素能递质机制的外周作用已得到综述。除了受体阻断作用外，β-肾上腺素能受体拮抗剂在高浓度时可能会抑制去甲肾上腺素的神经元摄取；抑制单胺氧化酶；抑制去甲肾上腺素摄取到递质储存囊泡中，并抑制去甲肾上腺素的神经元外摄取。高浓度的β-肾上腺素能受体拮抗剂（阈值约为30μM）也会从神经元内储存部位释放去甲肾上腺素；然而，它们的内在拟交感活性通常归因于其部分激动剂特性。β-肾上腺素能受体拮抗剂具有肾上腺素能神经元阻断活性以及奎尼丁样或局部麻醉活性。文中讨论了涉及突触前β-肾上腺素能受体的正反馈机制的存在。有人提出，β-肾上腺素能受体拮抗剂引起的心动过缓是由于循环中的儿茶酚胺或递质去甲肾上腺素在心脏接头外β-肾上腺素能受体部位的作用被阻断所致。
