The mode of action of indirectly acting sympathomimetic amines was analysed in the rat vas deferens (preloaded with <sup>3</sup>H-(–)-noradrenaline). When monoamine oxidase (MAO), catechol-O-methyltransferase and vesicular uptake were inhibited (i.e., when the concentration of <sup>3</sup>H-noradrenaline in the axoplasm was high), all substrates of neuronal uptake induced a carrier-mediated outward transport of ¾noradrenaline, in strict dependence on the K<sub>m</sub> for neuronal uptake of the substrate. However, when MAO and vesicular uptake were not inhibited, some of the substrates of neuronal uptake were better releasers of <sup>3</sup>H-noradrenaline than others; obviously, when the axoplasmic <sup>3</sup>H-noradrenaline concentration is very low (intact vesicular uptake, intact MAO), a ‘mobilization’ of vesicular <sup>3</sup>H-noradrenaline is a prerequisite for substantial release.