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IN 1964 Justin-Besançon and his co-workers described a new compound that depressed the vomiting center and stimulated gut motility.1 Metoclopramide (Fig. 1) (methoxychloroprocainamide [RegIan]) resulted from efforts to alter the procaine molecule so that its antiemetic properties would equal those of the phenothiazines.1 , 2 Like the phenothiazines, metoclopramide acts on the brain by blocking dopamine receptors: it induces extrapyramidal symptoms and stimulates prolactin secretion but has at best weak antipsychotic properties. Since metoclopramide and its congeners sulpiride, sultopride, and tiapride differ in some clinical and pharmacologic respects from other antipsychotic drugs, it has been suggested that these substituted benzamides act on . . .
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Koch‐Weser et al. (1981) studied this question.
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