Continuous electrical stimulation of the cut synpathetic innervation to perfused gracilis muscles restored vasoconstrictor tone and active dilatation resulted when stimulation was terminated. This dilatation was unaffected by cholinergic blockade but was blocked by the antihistamine tripelennamine. Prior vasoconstriction was not required to produce active dilatation since sympathetic stimulation applied during infusion of xylocholine (betaTM10) produced no vasoconstrictor response yet an antihistamine-sensitive vasodilatation appeared when stimulation ceased. This dilatation was also blocked by the alpha-adrenergic receptor blocker phentolamine even though adrenergic vasoconstrictor tone was absent. These results suggest that the release of histamine from its storage site is mediated by an alpha-receptor mechanism. Since betaTM10 abolished adrenergic vasoconstriction but preserved histamine-mediated vasodilatation that could be prevented by alpha-adrenergic blockade, it is proposed that histamine release may be under the control of separate adrenergic fibers without a vasoconstrictor function. This mechanism may underlie the process of active reflex vasodilatation since upon reflex withdrawal of tonic sympathetic activity an antihistamine-sensitive vasodilatation occurs.