Effect of prazosin on the efflux of 3H-norepinephrine and metabolites from the intima and adventitia of the rabbit ear artery.

The spontaneous and stimulation-induced (SI) effluxes of 3H-norepinephrine (3H-NE) and its metabolites from the intimal and adventitial surfaces of perfused segments of rabbit ear arteries were determined; vessels were previously incubated with 3H-NE (0.6 microM). The total SI adventitial efflux of 3H was approximately 10-fold greater than the intimal efflux, contained a higher percentage of unchanged 3H-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 microM) 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 3H-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 3H-NE and its intraneuronally formed metabolites across the media. Prazosin decreased the percentage of unchanged 3H-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 3H-NE.