Abstract
ABSTRACT Two women who had previously undergone pituitary stalk transection for cancer of the breast provided a unique model to test whether in human subjects TRH stimulates PRL release by direct action on the pituitary or by some secondary mechanism at the hypothalamic level. The completeness of stalk section was thoroughly documented in both patients. The intravenous administration of synthetic TRH caused a significant, though delayed, rise in PRL levels. Chlorpromazine, which induces PRL secretion by an effect on the hypothalamus, did not affect PRL levels. Thus, in human beings, TRH appears to stimulate PRL release by a direct action on the pituitary.
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