Metabolic fate of the sympathoneural imaging agent 6-[18F]fluorodopamine in humans.

We examined the metabolism of 6-[18F]fluorodopamine, by assaying arterial plasma concentrations of radioactivity, 6-[18F]fluorodopamine, and 6-[18F]fluorodopamine metabolites in untreated subjects or subjects given desipramine to block neuronal uptake of catecholamines or tyramine to displace vesicular amines. After the 3-min 6-[18F]fluorodopamine infusion, plasma 6-[18F]fluorodopamine levels declined precipitously, total radioactivity declining slowly. After 30 min, the main identified metabolite was 6-[18F]fluorodopamine-sulfate. Desipramine attenuated the rapid increase in plasma 6-[18F]fluorodihydroxyphenylacetic acid levels, and tyramine briefly increased 6-[18F]fluorodopamine levels. Neither drug affected 6-[18F]fluorodopamine-sulfate levels. The results indicate that soon after 6-[18F]fluorodopamine infusion, plasma radioactivity corresponds mainly to 6-[18F]fluorodopamine metabolites; that sympathetic nerves rapidly remove 6-[18F]fluorodopamine, which then undergoes oxidative deamination in the neuronal cytoplasm and sequestration in sympathetic vesicles; and that sulfoconjugation of [18F]fluorodopamine occurs extraneuronally.