Comparison of the effects of ethanol on beta-adrenergic receptors in heart and brain.

Low, physiologically-attainable concentrations of ethanol affect agonist binding to cerebral cortical and cardiac beta-adrenergic receptors. In cerebral cortex, ethanol decreases the affinity of the high-affinity state of the receptor for isoproterenol. This may reflect a direct action of ethanol on the receptor. Ethanol also potentiates the action of guanine nucleotides on agonist binding, suggesting a second site of action at Ns. In heart, ethanol increases the proportion of low-affinity binding sites, an effect which is similar to that of guanine nucleotides, and may also indicate an action of ethanol at Ns. After chronic ethanol ingestion, the total number of cardiac beta-adrenergic receptors is decreased, but the proportion of high-affinity sites is increased. This change could reflect an increased sensitivity to catecholamines. In cerebral cortex, chronic ethanol results in a single, low-affinity binding site for agonist, compatible with an "uncoupled" receptor. Such a change also occurs during homologous desensitization, and may result from increased norepinephrine turnover during chronic ethanol ingestion. The differential responses to ethanol of similar receptors in heart and brain exemplify the specificity of ethanol's actions on various organ systems.