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The beta-adrenoceptors are now well individualized. They are divided into three distinct units: the receptor site, a regulating protein and a catalytic unit. The receptor density of the cell membrane varies according to the degree of stimulation of the receptor by agonists or the degree of blockade by antagonists. The myocardial or lymphocytic beta-adrenoceptor density is measured by "radioreceptor" assay using a radioactive beta-blocker. The myocardial beta-receptor density falls during heart failure, mainly to the detriment of beta 1 receptors. The density of beta 2 receptors remains unchanged. This fall in beta 1 receptors is related to the increase in the circulating catecholamines (down regulation) and is proportional to the severity of the disease. These physiological and physiopathological consequences can be directly applied to the treatment of heart failure by positive inotopic drugs or by beta-blockers.
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