Effect of central nervous system dopaminergic activation on prolactin secretion in man: Evidence for a common central defect in hyperprolactinemic patients with and without radiological signs of pituitary tumors

P. G. Crosignani, C. Ferrari, A. Malinverni, C. Barbieri, A. M. Mattei, R. Caldara, M. Rocchetti

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Abstract

Previously, it has been shown that the PRL-suppressive effect of L-dopa is unchanged by carbidopa pretreatment in healthy subjects but is markedly impaired in patients with PRL-secreting tumors, suggesting that the inhibitory action of L-dopa is mediated through the central nervous system (CNS) in normal humans and peripherally in patients with prolactinomas. Also, it has been claimed that the administration of nomifensine, a drug which stimulates CNS but not pituitary dopamine receptors, inhibits PRL secretion in hyperprolactinemic patients without, but not with, evidence of pituitary tumors. To further evaluate the possible diagnostic applications of these tests, L-dopa (500 mg) alone and 100 mg plus 35 mg carbidopa after carbidopa pretreatment (50 mg every 6 h) or nomifensine (200 mg) were administered orally to healthy subjects and patients with hyperprolactinemia of different etiology. The mean serum PRL concentration was similarly inhibited in normal subjects by L-dopa alone and by carbidopa plus L-dopa (mean nadir levels, 33.6 ± 2.5% and 31.7 ± 2.8% of basal, respectively; n = 16), while in hyperprolactinemic patients, L-dopa alone was significantly more effective than the combined treatment in both patients with and without radiological evidence of pituitary tumors [n = 20 for each group; mean nadir of serum PRL levels, 32.5 ± 3.9% and 60.1 ± 4.6%, respectively in the tumor group (P

Original languageEnglish
Pages (from-to)1068-1073
Number of pages6
JournalJournal of Clinical Endocrinology and Metabolism
Volume51
Issue number4
Publication statusPublished - 1980

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ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

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