Uptake and metabolism of 3H-noradrenaline 0.18 mumol/l was examined in rabbit gingival slices and ear artery segments. The tissues were incubated with the 3H-amine for 30 min. The artery accumulated approximately ten times more of the 3H-amine and generated four times more 3H-metabolites than the gingiva. In both tissues, chronic sympathetic denervation resulted in marked decreases in 3H-noradrenaline accumulation and deamination. An inhibitor of sympathetic neuronal uptake, cocaine 30 mumol/l, strongly inhibited the firmly-bound component of 3H-noradrenaline accumulation by the tissues and strongly decreased the accumulation of deaminated metabolites in the incubating medium. It is concluded that the sympathetic nerve terminals play an important role in the accumulation and deamination of noradrenaline in the gingiva and in the artery. Chronic sympathetic denervation resulted in increased 3H-normetanephrine (NMN) formation by the gingiva and the artery, indicating that in both tissues the noradrenaline was O-methylated at sites extraneuronal to the sympathetic nerves. Differences between the effects of cocaine in the gingiva and artery, with respect to 3H-NMN accumulation in the incubating medium, are interpreted as evidence that in the gingiva, but not in the artery, cocaine inhibits extraneuronal O-methylation, as well as neuronal uptake, of noradrenaline.