Agents Which Block Adrenergic β-Receptors

Abstract

Adrenergic receptors can be described only in terms of effector response to the administration of certain chemical agents. The adrenergic [beta]-receptor, as originally described, responds best to isoproterenol and is associated with cardiac stimulation, vasodilation, and inhibition of smooth muscle in the bronchi, myometrium, and intestine. When the [beta]-receptor is restricted to this description, it can be uniformly found in practically all mammalian species, and in frogs and turtles. The adrenergic [beta]-receptor blocking agents, as exemplified by propranolol, competitively and specifically blocked the responses of the [beta]-receptor to isoproterenol, other endogenous or exogenous catecholamines, and all other sympathomimetic agents. The relationship between the [beta]-receptors and the metabolic responses to the catecholamines is not clearly defined. Isoproterenol is not the most potent catecholamine; in fact, in some cases, it is inactive as compared to epinephrine. Adrenergic [beta]-receptor blocking agents prevent the metabolic responses to epinephrine, but so do several adrenergic [alpha]-receptor blocking agents, and several methoxamine derivatives. The latter do not qualify as adrenergic [beta]-receptor blocking agents. It would be too restrictive to consider that adrenergic metabolic responses are controlled by adrenergic [beta]-receptor blocking agents. A3rd receptor may need to be considered, or the muscular responses may be due to the metabolic changes. The adrenergic [beta]-receptor blocking agents will have therapeutic use in any condition in which adrenergic [beta]-receptor activity is excessive or undesirable.