Effects of CNS dopamine augmentation on stimulated prolactin secretion.
The site, hypothalamic and/or pituitary, for dopaminergic inhibition of prolactin (PRL) secretion is unknown. Consequently, the effect of central dopamine (DA) augmentation on stimulated PRL release was determined in 5 healthy men. Regular insulin (o.1 U/kg i.v.), a potent central stimulus for PRL secretion, and TRH, a direct hypophyseal stimulus, were given alone or one hour after the third and fourth doses, respectively, of L-dopa plus the peripheral decarboxylase inhibitor, carbidopa (Sinemet 20/200 or 25/250 every 6 hours). PRL increased from 26.6 +/- 5.8 to 48.8 +/- 5.2 ng/ml (p less than 0.01) 40 minutes after insulin administration. In contrast, during Sinemet therapy the hypoglycemia-mediated PRL release did not occur, and the PRL levels were significantly lower than after insulin alone from 40 through 180 minutes. Following TRH, neither the maximal PRL rise (69.3 +/- 3.2, TRH alone vs 48.7 +/- 19.8 ng/ml, TRH + Sinemet) nor the maximal increment (37.5 +/- 5.5 vs 29.9 +/- 20.3 ng/ml) was significantly affected by Sinemet. It is concluded that central DA augmentation abolishes central but not peripherally mediated PRL release.
D000328:Adult; D002230:Carbidopa; D006801:Humans; D006834:Hydrazines; D007328:Insulin; D007980:Levodopa; D008297:Male; D011388:Prolactin / Q000378:metabolism*; D013973:Thyrotropin-Releasing Hormone
D006834:Hydrazines; D007328:Insulin; D007980:Levodopa; D013973:Thyrotropin-Releasing Hormone; D011388:Prolactin; D002230:Carbidopa