Dopaminergic Inhibition of Prolactin Secretion in Patients with Prolactin-Secreting Pituitary Tumors

(6 male, 4 female) and 8 patients with hyperprolactinemia associated with pituitary tumors were given L-dopa, 0.5 g alone, or 0.1 g after a 24-h pretreatment with carbidopa, 50 mg every 6 h, which produces peripheral dopa decarboxylase inhibition. Similar degrees of PRL suppression were observed in normal subjects (basal plasma PRL 13+2 ng/ml) after L-dopa alone (48±+4%) and after L-dopa plus carbidopa (58+6%). In patients with pituitary tumors and elevated plasma PRL (73+14 ng/ml), L-dopa alone led to PRL suppression comparable with that in normal subjects (47±+6%). However, L-dopa plus carbidopa resulted in only minimal suppression of plasma PRL (19+4%) which was significantly less than after L-dopa alone (P < 0.001). Urinary homovanillic acid excretion, which reflected peripheral dopa decarboxylation was similar in controls and tumor patients after L-dopa both alone and after carbidopa pretreatment. Comparable suppression ofPRL levels in response to a dopamine infusion (4 jig/kg per min for 3 h) was observed in controls and tumor patients. The results indicate that although peripheral conversion of exogenous dopa to dopamine can suppress PRL secretion, in normals, the central nervous system conversion of dopa to dopamine in the presence of peripheral dopa decarboxylase inhibition is sufficient to account for its PRL-suppressive effects. In contrast, patients This work was presented in part at the AFCR National Meeting, Washington, D. C., 1 May 1977. Received for publication 28 July 1977 and in revised form 21 November 1977. with tumors, while retaining peripheral dopaminergic inhibitory effects on PRL secretion, exhibit a marked reduction of central dopaminergic inhibition of PRL