Effect of two indirectly acting dopamine agonists on prolactin secretion in normo- and hyperprolactinemic subjects: comparison with the effect of nomifensine

The effect on plasma prolactin (PRL) of two indirectly acting DA agonists (IADA), i.e. methylphenidate and amineptine was studied in normo- and hyperprolactinemic subjects. PRL responses to methylphenidate and amineptine were compared to those previously obtained with the use of another IADA, namely, nomifensine. In normoprolactinemic women methylphenidate (20 mg, orally) or amineptine (200 mg, orally) induced a significant decrease in baseline PRL. (maximal change from baseline 50% at 90 min). a pattern reminiscent of that induced by nomifensine (maximal change from baseline 35% at 120 min). Likewise, in puerperal women (postpartum day 2) methylphenidate and amineptine induced a clear-cut lowering of baseline PRL (40% inhibition at 90 min and 180 min. respectively): nomifensine induced 60% inhibition of resting PRL levels at 150 min. In subjects with pathological hyperprolactinemia (proven or highly probable PRL-secreting tumor or uncertain etiology), previously shown to be unresponsive to the PRL-lowering effect of nomifensine, methylphenidate or amineptine did not significantly lower baseline PRL (maximal change from baseline 8% at 150 min and 3% at 90 min, respectively). In few of these subjects methylphenidate and amineptine failed to lower plasma PRL levels also at doses of 30 and 300 mg, orally, respectively. These data indicate that (1) two other I ADA, i.e., methylphenidate and amineptine, are effective PRL-lowering agents in both normoprolactinemic and puerperal subjects, whereas they are unable to lower plasma PRL in patients with proven or probable PRL-secreting tumors; (2) the ability of the different drugs to inhibit plasma PRL in puerperal versus pathological hyperprolactinemia emphasizes the different tuberoinfundibular DA (TIDA) neurotransmission present in the two clinical conditions; (3) in view of the mechanism of action of the IADA, there is a defect in TIDA metabolism or transport in patients harboring a prolactinoma. © 1981 S. Karger AG, Basel.