The effect of changing endocrine status on the uterine endometrium of the female Fischer rat was observed in vivo after neonatal androgenization, after aging, after estrogen (E) implant in ovariectomized (OVX) rats, and in vitro after progesterone (P) addition to monolayer cultures of uterine tumor cells. Neonatal androgenization produced cystic ovarian follicles and persistent vaginal cornification for 10-14 mo, indicative of an anovulatory, persistent E status. The constant estrous (CE) state, induced by androgenization, uniformly produced focal glandular hyperplasia of the endometrium at 9 mo of age. Focal glandular hyperplasia, which was absent in the cycling 6-mo-old estrous endometrium, was also apparent in the 12-mo-old rats which had ceased cycling and entered natural CE. Subcutaneous estradiol-17 beta (E2) implants in 12-mo-old OVX rats induced early cystic and adenomatous changes in the foci of hyperplasia. Acyclic control rats, 21 mo old, in persistent diestrus (PD) exhibited a 3-fold elevation of serum P associated with glandular atrophy of the endometrium. Ten nM P also inhibited proliferation of endometrial cells in cultures prepared from tumors of 21-mo-old rats. On the other hand, adenomatous hyperplasia was observed in 29-mo-old PD rats, despite the presence of low serum E and elevated serum P. These results indicate that either induced or natural constant E status leads to focal glandular hyperplasia in the Fischer rat. E2 implants in the 12-mo-old OVX Fischer rat induced early cystic and adenomatous changes in the focal hyperplasia. Inhibition of these focal hyperplasias was associated with elevated serum P at 21 mo. The development of adenomatous hyperplasia in the aged endometrium, on the other hand, occurred despite elevated serum P at 29 mo.
The role of 17 beta-estradiol (E2) in the modulation of N6,O2'-dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP)-induced hormone release was examined in pituitary monolayer cultures prepared from intact and ovariectomized female rats. Incubations with 5 mM DBcAMP for 4 h significantly (P less than 0.05) stimulated both luteinizing hormone (LH) and prolactin (PRL) release in pituitary cultures prepared from rats at diestrus and from cycling rats at random stages of the estrous cycle. However, DBcAMP failed to stimulate the LH or PRL release in cultures prepared from ovariectomized rats in which the basal LH and PRL release was approximately three-fold and one-tenth of that in cycling rats, respectively. Pretreatment with 1 nM E2 augmented or restored the DBcAMP-induced LH release but not the DBcAMP-induced PRL release in cultures prepared from cycling or ovariectomized rats, respectively. Furthermore, E2 treatment alone of cultures prepared from cycling rats significantly increased intracellular cAMP concentrations and cAMP-binding activities by at least twofold over that of the non-E2-treated controls. The E2-induced rise in cellular cAMP concentration preceded the E2-induced rise in cAMP binding. These results indicate that the priming effect of E2 on pituitary LH responsiveness to DBcAMP is associated with increased cAMP production and cAMP binding.
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