Prolactin Response to Acute Administration of Different L-Dopa plus Decarboxylase Inhibitors in Parkinson’s Disease

Abstract

Plasma prolactin (PRL) level modifications after acute administration of L-dopa, L-dopa plus carbidopa and L-dopa plus benserazide were studied in parkinsonian patients. PRL increase after benserazide was compared with PRL response after carbidopa at the same dosage in untreated parkinsonian patients. A further study of the hyperprolactinemic effect of benserazide was performed in vitro on isolated and dispersed rat pituitary cells. Benserazide-induced hyperprolactinemia in parkinsonian patients could be due to a direct effect of the drug at the hypothalamic level and consequently to an inhibition of dopamine decarboxylation in the tuberoinfundibular dopaminergic system. Benserazide may possibly exert its biological activity through the production of active metabolites in vivo.