Abstract

Human pituitary prolactin (PRL) is released in a pattern that is different from growth hormone (HGH). Basal PRL concentrations remain unchanged throughout the menstrual cycle and bear no apparent relationship to the cyclic change in gonadotropins. Significant increases in PRL occur after intramuscular chlorpromazine (CPZ). The response is dose related. These results correlate with PRL values measured in patients ingesting large amounts of phenothiazines for psychiatric disease. Thyrotropin-releasing hormone (TRH) provokes the release of PRL as well as thyroid-stimulating hormone (TSH). TRH-induced PRL release during menses is similar to that found at midcycle. On the other hand, HGH secretion remains unaffected by CPZ and TRH. Throughout pregnancy, basal plasma PRL rises to a mean of 214 ng. per milliliter at term. In spite of this, PRL levels rise even higher in response to intravenous TRH. Postpartum, puerperal PRL levels increase in response to nursing and intravenous TRH but not after intranasal oxytocin. The post-TRH response can be dissociated from the PRL response to nursing especially beyond 60 postpartum days. Elevations in endogenous PRL secretion are followed by changes in breast function within three hours. These changes include engorgement with increased milk production and letdown. No such changes occur after intravenous TRH in pregnancy. Intravenous TRH appears to be a specific stimulus to PRL release and is without significant side effects. These studies suggest that PRL may promote breast milk production in lactating women. The mammary response to elevated PRL concentrations may be modified, however, by the concentration of endogenous estrogen and progesterone since no breast engorgement followed the post TRH-PRL rise before delivery. There is no similarity between the secretion of PRL and HGH in pregnancy.

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