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The involvement of the adrenergic system derived from locus ceruleus (LC) in the regulation of blood-brain barrier has been recognized to be mediated to a large extent by the endothelium.1,6 These cells, which produce many vasoactive and inflammatory substances, have been shown to participate in the interaction between immune cells and the central nervous system (CNS). For example, the infiltration of inflammatory cells into the CNS, a critical step in the pathogenesis of many CNS diseases, is limited in normal brain. In inflammation, the endothelium has been recognized as an active participant in pathogenic mechanisms by its capacity to express adhesion molecules. These molecules facilitate binding with circulatory leukocytes, which may result in their activation and ultimate passage across the endothelium. In addition, tumor necrosis factor-α (TNFα) is one of the most important endogenous cytokines that mediates local inflammation. Its proinflammatory activities toward vascular endothelium have also been described previously.2,7 Many reports also suggest that the changes in BBB properties in neurological disorders may be associated with disturbances of adrenergic input.3,4 Thus, we examined the influence of adrenergic agents on TNFα-induced intercellular adhesion molecule-1 (ICAM-1) on human brain microvascular endothelial cells (HBEC).