Effects of β-Adrenoreceptor Blocking Drugs on Adrenergic Transmission

Abstract

TThe peripheral actions of β-adrenoreceptor antagonists on adrenergic transmitter mechanisms have been reviewed. In addition to receptor blockade, β-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 nor adrenaline. High concentrations of β-adrenoreceptor antagonists (threshold about 30μM) also release noradrenaline from intraneuronal stores; however, their intrinsic sympathomimetic activity is generally attributed to their partial agonist property. β-Adrenoreceptor antagonists possess adrenergic neurone blocking activity and quinidine-like or local anaesthetic activity. The existence of a positive feedback mechanism involving prejunctional β-adrenoreceptors is discussed. It is suggested that bradycardia produced by β-adrenoreceptor antagonists is due to blockade of the action of circulating catecholamines or of transmitter noradrenaline at cardiac extrajunctional β-adrenoreceptor sites.