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The purported dopamine agonist DPI inhibits [3H]noradrenaline release from rat cortical slices but not [3H]dopamine and [14C]acetylcholine release from rat striatal slices in‐vitro

The effects of the purported dopamine (DA) receptor agonist (3,4‐dihydroxyphenylimino)‐2‐imidazolidine (DPI) upon the in‐vitro K+‐induced release of [3H]DA and [14C]acetylcholine from rat neostriatal slices, and of [3H]noradrenaline from rat neocortical slices have been investigated and compared with those of the DA receptor agonist TL‐99 and the α‐adrenoceptor agonist clonidine, respectively. The rapid decomposition of the catechol compounds DPI and TL‐99 in the Krebs‐Ringer bicarbonate superfusion medium was shown to be inhibited by both the chelating agent EDTA and the reducing agent ascorbic acid. The results suggest that in‐vitro DPI is unable to stimulate striatal DA receptors, whereas it is effective in stimulating cortical α2‐adrenoceptors (EC50 = 61 nm). It is concluded that DPI should be considered as a mixed α1/α2‐adrenoceptor agonist and that the designation of DPI as a DA receptor agonist should be abandoned.