Hoffman P L, Valverius P, Kwast M, Tabakoff B
National Institute on Alcohol Abuse and Alcoholism, Division of Intramural Clinical and Biological Research, Bethesda, MD 20892.
Alcohol Alcohol Suppl. 1987;1:749-54.
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.
生理上可达到的低浓度乙醇会影响激动剂与大脑皮质及心脏β-肾上腺素能受体的结合。在大脑皮质中，乙醇会降低受体高亲和力状态对异丙肾上腺素的亲和力。这可能反映了乙醇对受体的直接作用。乙醇还会增强鸟嘌呤核苷酸对激动剂结合的作用，表明在Ns存在第二个作用位点。在心脏中，乙醇会增加低亲和力结合位点的比例，这一效应与鸟嘌呤核苷酸的效应相似，也可能表明乙醇在Ns存在作用。长期摄入乙醇后，心脏β-肾上腺素能受体的总数会减少，但高亲和力位点的比例会增加。这种变化可能反映了对儿茶酚胺的敏感性增加。在大脑皮质中，长期摄入乙醇会导致激动剂出现单一的低亲和力结合位点，这与“解偶联”受体相符。这种变化在同源脱敏过程中也会发生，可能是由于长期摄入乙醇期间去甲肾上腺素周转率增加所致。心脏和大脑中相似受体对乙醇的不同反应体现了乙醇对各种器官系统作用的特异性。
