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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Regulation of prolactin secretion in patients with Cushing's disease. A comparative study on the effects of dexamethasone, lysine vasopressin and ACTH on prolactin secretion by the rat pituitary gland in vitro.

In 15 untreated patients with Cushing's disease the regulation of prolactin (PRL) was evaluated. Plasma PRL was 11.5 +/- 4.8 vs. 5.3 +/- 3.6 ng/ml (patients with Cushing's disease vs. control; mean +/- S.D.; p less than 0.001). The maximal increment of plasma PRL in response to TRH was 32.3 +/- 17.3 vs. 27.9 +/- 17.2 ng/ml (NS); the maximal increment of plasma PRL in response to an insulin-induced hypoglycemia was 3.8 +/- 4.6 vs. 22.7 +/- 12.4 ng/ml (p less than 0.001). Additionally the effect of dexamethasone, lysine vasopressin and ACTH on the secretion of PRL by rat pituitary glands in vitro was studied. Dexamethasone (1.25--10 microM) inhibited the secretion of PRL. However, in the presence of dexamethasone modulation of PRL release by TRH and dopamine remained unaltered. Lysine vasopressin (5 nM - 5 microM) and ACTH (0.5--12.5 microM) did not have a direct effect on PRL release by normal rat pituitary glands in vitro and these substances also did not interfere with dopamine-mediated inhibition of PRL release. Conclusions: In Cushing's disease the PRL responses to TRH (normal) and to insulin-induced hypoglycemia (blunted) are differentially affected. Therefore, hypercortisolism probably selectively interferes with the regulation of PRL secretion at a suprahypophyseal level. It is concluded that TRH and dopamine regulate PRL release at sites which are not under corticosteroid regulation, while corticosteroids modulate PRL secretion in response to stress.[1]


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