Effects of Indomethacin and Prostaglandin Injections on Plasma Prolactin and Growth Hormone Levels in Rats*
- 1 February 1978
- journal article
- research article
- Published by The Endocrine Society in Endocrinology
- Vol. 102 (2), 531-539
- https://doi.org/10.1210/endo-102-2-531
Abstract
Ovariectomized (OVX) rats were injected with estradiol benzoate (Eb, 2 .mu.g s.c.) and 2 days later their plasma PRL [prolactin] and GH [growth hormone] 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 Eb-induced PRL release and the pulsatile GH release in a dose-related manner. Intraventricular injection of 9 different prostaglandins (PG) and 2 endoperoxide analogs in conscious, free-moving OVX, Eb-treated rats revealed that only PGE1 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 PGE2, which had been ineffective in rats not treated with Id. Id-treated rats also showed a striking increase in plasma PRL after the i.v. injection of PGE1. This increased PRL response to PG seemed to reside at a pituitary level because the PRL response to TRH [thyroid releasing hormone] was also enhanced in Id-treated rats. Pituitary GH response to TRH was blunted by ID treatment. 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.This publication has 9 references indexed in Scilit:
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