Alterations in β-adrenergic receptor binding during ethanol withdrawal

Abstract

CHARACTERISTIC features of ethanol withdrawal, including tremor, agitation, seizures, tachycardia and increased blood pressure, frequently develop in chronic alcoholics 6–60 h after the discontinuation of long-term heavy ethanol consumption^1–4. Similar symptoms are seen in hyperadrenergic states such as anxiety and thyrotoxicosis^5,6. There is evidence to suggest that augmented sensitivity to catecholamines in thyrotoxicosis is due to the development of β-adrenergic receptor supersensitivity in cardiac and skeletal muscle cell surfaces^7–10. Propranolol, a β-adrenergic blocker, has been shown to control some of the clinical signs of ethanol withdrawal, such as arrhythmia, hypertension and tremor^11–13. In addition, propranolol significantly decreases urinary excretion of noradrenaline during ethanol withdrawal¹⁴. These findings have led to the suggestion that peripheral manifestations of increased adrenergic activity in ethanol withdrawal are secondary to increased sympathetic neural outflow and that this increase in central catecholaminergic outflow may be the result of increased β-adrenergic receptor sensitivity in the alcohol withdrawal state in man¹⁴. We report here attempts to determine whether increased central and peripheral β-adrenergic receptor binding could be demonstrated in rats during ethanol withdrawal.