Does Bromocriptine Block Thyrotropin-Releasing Hormone-Induced Prolactin Release during Pregnancy?*

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Abstract
PRL responses to 200 µg of iv TRH were measured in 16 healthy women with normal early pregnancy before and at the end of bromocriptine treatment of 5.0–7.5 mg daily for 1–2 weeks. Before the start of bromocriptine, TRH caused a PRL elevation from 19.1 ± 2.2 to 95.2 ± 12.6 ng/ml (mean ± SE) after 20 min, with a mean maximal PRL increment of 71.7 ± 11.6 ng/ml. Bromocriptine suppressed basal plasma PRL level to 3.6 ± 0.8 ngng/ml (P < 0.001). TRH then caused a PRL rise to 18.8 ± 1.8 ng/ml at 20 min, with a mean maximal PRL increment of 15.7 ± 1.8 ng/ ml. The absolute PRL response was significantly smaller (P < 0.001) during bromocriptine intake than before, whereas the mean percent increments in PRL levels after TRH administration were similar in the presence and absence of bromocriptine. Fifteen of these women were restudied with TRH stimulation 4–6 weeks after legal abortion, and the PRL responses to TRH were normal. When 7 of these women were once again treated with bromocriptine and retested with TRH, no absolute or relative PRL response to TRH emerged. These results indicate that the effect of bromocriptine on TEH-induced PRL release differs between the pregnant and nonpregnant states.

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