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Action of an estrogen antagonist in intact and ovariectomized rats

1973; Elsevier BV; Volume: 7; Issue: 3 Linguagem: Inglês

10.1016/0010-7824(73)90014-0

1879-0518

Kenneth W. Perry, Gene DiPasquale, E. Ferguson, Charles Pozzi, Charles L. Rassaert,

Stress Responses and Cortisol

The uterine uptake of tritiated estradiol-17β, at both low (0.6 μg/ kg) and high doses (2.4 μg/kg), in intact or ovariectomized immature rats was inhibited in a dose-related manner by the estrogen antagonist, CN-55,945-27 (l-(2-&p-[α(p-methoxyphenyl)-β-nitrostyryl]-phenoxy&-ethyl)-pyrrolidine monocitrate). With low dose estrogen treatment, CN-55,945-27 did not inhibit estradiol-17β-induced uterine weight increases in the intact rats. However, in the ovariectomized rats, the high dose of CN-55, 945-27 inhibited the low dose estrogen stimulation of uterine weight increase. When the high dose of estrogen was used, a direct correlation existed between the CN-55,945-27 dose-related reduction of the uptake of the tritiated estradiol-17β and its inhibition of the estrogen induced uterine growth in both the intact and ovariectomized rats. These data and the differences observed between the intact and ovariectomized rats in the uterine uptake of tritiated estradiol-17β and in the degree of stimulation over the control uterine weights suggest that a combination of the presence of endogenous estrogen or other substances (intact rats) and an alteration of the affinity of the uterine estrogen receptors are involved. The patterns of uptake of tritiated estradiol-17β by the pituitaries in the intact and ovariectomized rats and of the inhibition of this uptake by CN-55,945-27 were similar to those observed for the uteri. Uptake of tritiated estradiol-17β by the hypothalami and the effect of CN-55,945-27 on this uptake did not produce the same patterns observed for the uteri and pituitaries. Differences in the hypothalamic estrogen uptake between the intact and ovariectomized rats were not evident. CN-55,945-27 inhibition of this hypothalamic estrogen uptake occurred only in the intact rats treated with the high dose of estradiol-17β. These data indicate that there is an ovarian (?) substance(s) which regulates the sensitivity or affinity of the uterine and pituitary estrogen receptors and which can regulate the action of estrogen antagonists in the hypothalamus in immature rats.