Since the early observations of Carl Ludwig that the sympathetic nervous system exerts a tonic influence on resistance vessels, many additional factors have been identified which control vascular tone. The active modulator role of endothelium-derived nitric oxide (NO) in this process has emerged only in the last decade. The interaction of the local vasodilator, NO, with systemic alpha-adrenergic control of vascular tone as well as with pressure-induced myogenic vasoconstriction is briefly reviewed in the present paper. Cellular mechanisms of this interaction are discussed. In vitro and in vivo experiments indicate that the continuous basal release of NO potently attenuates alpha-adrenergic and myogenic tone in resistance vessels by several independent mechanisms and that endothelial impairment results in abnormal vasoconstriction.