Pituitary hormones and prolactin-releasing activity in rats with primary estrogen-induced pituitary tumors

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Abstract

Pituitary tumors were induced in Wistar-strain female rats by repeated injections of depot estradiol preparations. Fifty-five, 130, and 200 days after the last injection, eight or nine experimental animals and the same number of untreated control animals were sacrificed. Pituitary weight, histology, and content of DNA, PRL, GH, TSH, and LH, hypothalamic content of PRL-releasing activity (PRL-RA) and immunoreactive TRH, and serum levels of PRL, GH, TSH, LH, T3, T4, and estradiol were determined. The pituitaries in the estrogen-treated rats increased markedly in weight and DNA content, and formed tumors. There was a striking increase in serum levels of PRL and a less marked increase in PRL content of the pituitary. Hypothalamic PRL-RA was higher than in the controls 55 and 200 days after the last estrogen injection at a time when serum estradiol levels were similar to those of controls. On the other hand, TSH, LH, and, to a slight degree, GH were suppressed. Short term administration of estrogen resulted in an increase of the serum level and pituitary content of PRL, an increase in the hypothalamic content of PRL-RA, as well as a decrease of the serum level and pituitary content of TSH. These results suggest that 1) excessive release of PRL from an estrogen-induced pituitary tumor is, at least in part, caused by excessive production of PRL-RA, 2) excessive GH release is not a general feature of primary estrogen-induced pituitary tumors, 3) the production and release of TSH in the pituitary is suppressed in rats with primary estrogen-induced pituitary tumors, probably due to hyperprolactinemia, and 4) the serum levels of GH, TSH, and LH tend to be maintained at the expense of the pituitary content of the respective hormone. © 1980 by The Endocrine Society.

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Nakagawa, K., Obara, T., & Tashiro, K. (1980). Pituitary hormones and prolactin-releasing activity in rats with primary estrogen-induced pituitary tumors. Endocrinology, 106(3), 1033–1039. https://doi.org/10.1210/endo-106-3-1033

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