Ovariectomized (OVX) rats were injected with estradiol benzoate (Eb, 2 μg sc) and 2 days later their plasma PRL and GH titers were determined in jugular blood samples drawn through an indwelling silastic cannula at 1- to 2-h intervals from 1000–1600 h. PRL was low in the morning and increased in the afternoon. Control OVX rats treated with oil did not show such an increase. Although Eb increased basal GH levels, plasma GH varied in a pulsatile manner in both OVX and OVX, Eb-treated rats. Indomethacin (Id), an inhibitor of prostaglandin synthesis administered 24 h before blood sampling, depressed the Ebinduced PRL release and the pulsatile GH release in a dose-related manner. Intraventricular injection of nine different prostaglandins (PGs) and two endoperoxide analogs in conscious, free-moving OVX, Eb-treated rats revealed that only PGEi released PRL and that both PGE1 and PGE2 released GH within 15 min of their injection. When [3H]PGE2 was injected intraventricularly < 3% of the injected radioactivity was found in the pituitary, 5, 10, and 15 min after injection. Intraventricular injection of PGE1 or PGE2 in Id-treated rats increased plasma GH levels as much as in control rats. In the case of PRL, the increase was much more pronounced. Plasma PRL levels were not only elevated by PGE1 but also by PGE2which had been ineffective in rats not treated with Id. Id-treated rats also showed a striking increase in plasma PRL after the iv injection of PGEi. This increased PRL response to PGs seemed to reside at a pituitary level because the PRL response to TRH was also enhanced in Id-treated rats. By contrast, pituitary GH response to TRH was blunted by Id treatment. The results suggest that hypothalamic PGE1 and PGE2 may be physiological components of the mechanisms responsible for estrogen-induced PRL release and for pulsatile GH secretion in the rat.
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