The infusion of small amounts of noradrenaline for short periods of time into reserpinized dogs restores the pressor action of tyramine if the latter is given during the infusion but not immediately thereafter. These findings are consistent with the hypothesis that tyramine acts on its own but requires for its action the presence of noradrenaline at the receptor sites, for under these circumstances there are no stores from which noradrenaline can be released. In the normal animal, or in a reserpinized animal after repletion of the stores by prolonged noradrenaline infusion, tyramine is envisaged to act by releasing from the stores a sufficient amount of noradrenaline which in turn “catalyses” the action of tyramine at the receptor sites. These results do not support the view that tyramine, like guanethidine, acts solely by virtue of the amount of noradrenaline it releases.