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. 1982 Aug 15;143(8):883-7.
doi: 10.1016/0002-9378(82)90467-7.

Integrity of central dopaminergic system in women with postpartum hyperprolactinemia

Integrity of central dopaminergic system in women with postpartum hyperprolactinemia

R Rao et al. Am J Obstet Gynecol. .

Abstract

In order to elucidate the role of elevated prolactin (PRL) on the central dopaminergic systems, the suppressive effects on PRL were studied after the administration of L-dopa and L-dopa plus carbidopa on consecutive days to the following three groups: 10 normoprolactinemic subjects, six nonnursing normal puerperal women, and seven hyperprolactinemic women without any evidence of pituitary tumor. In the normoprolactinemic subjects (basal PRL 13 +/- 2 ng/nl mean +/- SE), the suppressive effects of L-dopa alone and L-dopa plus carbidopa were similar (48% +/- 4% and 58% +/- 6%, respectively). In puerperal hyperprolactinemic subjects, the basal PRL (116.8 +/- 16.4 ng/ml) was suppressed 77% +/- 2% after administration of L-dopa and 51% +/- 7% after L-dopa plus carbidopa, significantly different from that of L-dopa alone (p less than 0.005), but similar to that observed in normal subjects. In the patients with idiopathic hyperprolactinemia, the baseline PRL (131 +/- 38 ng/ml) decreased 56.3% after the administration of L-dopa. In the presence of peripheral dopa decarboxylase inhibition, the administration of L-dopa decreased plasma PRL values 30%, a drop significantly different from that of L-dopa alone (p less than 0.02). Women with idiopathic hyperprolactinemia exhibit reduced central dopaminergic inhibition of PRL secretion similar to that in patients with pituitary tumor; whereas the response to central dopaminergic inhibition in postpartum women with comparable baseline PRL levels is similar to that in normoprolactinemic subjects. This indicates that hyperprolactinemia per se is not associated with a state of reduced central dopaminergic inhibition. The increased pituitary sensitivity to L-dopa observed in puerperal women may be due to alterations in PRL receptors or vascularity.

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