Jan 1, 1976

Effects of beta-adrenoreceptor blocking drugs on adrenergic transmission

Drugs
M J RandM W McCulloch

Abstract

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.

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Mentioned in this Paper

Reversible Inhibitors of Monoamine Oxidase
Depression, Chemical
Bradycardia
Sympathetic Nervous System
Neurosteroids
Neurons
Uptake
Catecholamines Measurement
Synaptic Transmission
Monoamine Oxidase [PK]

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