We have tested several prostaglandins (PGs) for effects on basal and TRH-induced TSH secretion in anesthetized female rats. The PGs were given intravenously or were stereotaxically injected directly into the medial basal hypothalamus or anterior pituitary. Plasma TSH levels were measured by radioimmunoassay. PGs A,, Bi, E,, and FlQ were tested at a dose of 20 µg⁄lOOg body wt intravenously and 2 µg⁄rat for stereotaxic injections. At these doses, these PGs were without effect on TSH secretion when given alone. However,all of the PGs potentiatedthe response of the pituitary to subsequently administered TRH. Thiseffect was observed onlyif the PGs were injected directly into the anterior pituitary. When administered intravenously, all the PGs failed to exhibit this effect, and one of them (PGEi) actually inhibited the response to TRH. This appears to be secondary to the cardiovascular effects of the PG that are evident at the dose used intravenously. It is concluded that, in spite of the fact that the PGs can not elicit TSH secretion in vivo, they may play a more subtle role in the regulation of TSH secretion as indicated by their potentiation of the stimulatory effect of TRH. (Endocrinology95: 1392, 1974)

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