Abstract
The effect of chlorpromazine on the metabolism of 3H-noradrenaline (3H-NA) released spontaneously or by electrical-field stimulation was studied on the rabbit isolated aorta preloaded with 3H-NA. Chlorpromazine (10(-6) M) neither altered the spontaneous outflow of total tritium nor had any major effect on the distribution of the 3H-outflow on 3H-NA and its 3H-metabolites. Chlorpromazine (10(-6) M) altered the distribution in stimulation-evoked 3H-overflow. Thus, 3H-NA and 3H-NMN were increased, 3H-DOPEG was markedly decreased and 3H-DOMA and 3H-OMDA were unchanged. It is concluded that chlorpromazine is an inhibitor of uptake-1.
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