26 November 2008
Previous studies in Rhesus monkeys have demonstrated that a dopamine (DA) infusion rate of 0.1 µg/kg·min induces peripheral DA levels similar to those measured in hypophysial stalk blood and normalizes serum prolactin (PRL) levels in stalk-transected animals. We therefore examined the effect of such DA infusion rate on basal and thyrotropin-releasing hormone (TRH)-stimulated PRL secretion in both normal cycling women and women with pathological hyperprolactinemia. 0.1 µg/kg·min DA infusion fully normalized PRL serum levels in 8 normal cycling women whose endogenous catecholamine synthesis had been inhibited by α-methyl- p-tyrosine (AMPT) pretreatment. Furthermore, DA significantly reduced, but did not abolish, the rise in serum PRL concentrations induced by both acute 500 mg AMPT administration and 200 µg intravenous TRH injection in normal women. A significant reduction in serum PRL levels in response to 0.1 µg/kg·min DA, similar to that observed in normal cycling women when expressed as a percentage of baseline PRL, was documented in 13 amenorrheic patients with TRH-unresponsive pathological hyperprolactinemia. However, a marked rise was observed in the serum PRL of the same patients when TRH was administered during the course of a 0.1-µg/kg·min DA infusion. The PRL response to TRH was significantly higher during DA than in basal conditions in hyperprolactinemic patients, irrespective of whether this was expressed as an absolute increase (Δ PRL 94.4 ± 14.2 vs. 17.8 ± 14.1 ng/ml, p < 0.002) or a percent increase (Δ% PRL 155.4 ± 18.9 vs. 17.9 ± 7.1, p < 0.0005), and there was a significant linear correlation between the PRL decrements induced by DA and the subsequent PRL responses to TRH. 1 A preliminary report of this investigation was presented at the National Meeting ‘Giornate Endocrinologiche Pisane’, Pisa, 1983. This research was supported in part by the Italian National Research Council (CNR) grant No. 82.02142. DA and TRH Interactions in the Control of PRL Release 203 These data would seem to show that the 0.1-µg/kg·min DA infusion rate reduces basal PRL secretion and blunts, but does not abolish, the PRL response to both TRH and acute AMPT administration. The strong reduction in PRL secretion and the restoration of the PRL response to TRH by 0.1 µg/kg·min DA infusion in the high majority of hyperprolactinemic patients, seem to indicate that both PRL hypersecretion and abnormal PRL response to TRH in women with pathological hyperprolactinemia are due to a relative DA deficiency at the DA receptor site of the pituitary lactotrophs.