The spontaneous and stimulation-induced (SI) effluxes of <sup>3</sup>H-norepinephrine (<sup>3</sup>H-NE) and its metabolites from the intimal and adventitial surfaces of perfused segments of rabbit ear arteries were determined; vessels were previously incubated with <sup>3</sup>H-NE (0.6 µM). The total SI adventitial efflux of <sup>3</sup>H was approximately 10-fold greater than the intimal efflux, contained a higher percentage of unchanged <sup>3</sup>H-NE (48 vs. 12%) and a lower percentage of O-methylated metabolites (17 vs. 55%); there was little difference between the percentages of deaminated catechols (35 vs. 31 %). Prazosin, at a concentration (0.24 µM) which prevented the arteries constricting during stimulation, had little effect on the composition of the SI effluxes; however, it caused 2- to 3-fold increases in the effluxes of <sup>3</sup>H-NE and its metabolites into the lumen during the period of stimulation. This effect is attributed to the failure of the vessel wall to thicken during stimulation, thus facilitating diffusion of <sup>3</sup>H-NE and its intra-neuronally formed metabolites across the media. Prazosin decreased the percentage of unchanged <sup>3</sup>H-NE and increased that of the deaminated catechols in the spontaneous efflux; these effects are attributed to a direct effect of prazosin on the intra-neuronal metabolism of <sup>3</sup>H-NE.