ABSTRACT
The present study was designed to assess the effects of bromocriptine, a dopamine agonist, on pituitary wet weight, number of immunoreactive prolactin cells and serum prolactin concentrations in estradioltreated rats. Ovariectomized Wistar rats were injected subcutaneously with sunflower oil vehicle or estradiol valerate (50 or 300 mug rat-1 week-l) for 2, 4 or 10 weeks. Bromocriptine (0.2 or 0.6 mg rat-1 day-l) was injected daily during the last 5 or 12 days of estrogen treatment. Data were compared with those obtained for intact control rats. Administration of both doses of estrogen increased serum prolactin levels. No difference in the number of prolactin cells in rats treated with 50 mug estradiol valerate was observed compared to intact adult animals. In contrast, rats treated with 300 mug estradiol valerate showed a significant increase in the number of prolactin cells (P<0.05). Therefore, the increase in serum prolactin levels observed in rats treated with 50 mug estradiol valerate, in the absence of morphological changes in the pituitary cells, suggests a "functional" estrogen-induced hyperprolactinemia. Bromocriptine decreased prolactin levels in all estrogen-treated rats. The administration of this drug to rats previously treated with 300 mug estradiol valerate also resulted in a significant decrease in pituitary weight and number of prolactin cells when compared to the group treated with estradiol alone. The general antiprolactinemic and antiproliferative pituitary effects of bromocriptine treatment reported here validate the experimental model of estrogen-induced hyperprolactinemic rats.
Subject(s)
Rats , Animals , Female , Bromocriptine/pharmacology , Estradiol/therapeutic use , Hyperprolactinemia/chemically induced , Ovariectomy , Pituitary Gland/drug effects , Pituitary Gland/physiology , Prolactin/blood , Prolactin/drug effects , Rats, WistarABSTRACT
The aim of the present work was to study the effects of the antiestrogen tamoxifen 9TAM) of progestin noresthisterone acetite (NA) and of their combination on serum prolactin levels, uterine growth and the presence of uterine immunoreactive prolactin estradiol- treated rats. Ovariectomized female Wistar rats were injected sc with estradiol valerate (VE, 50 µg/rat per week) or oil vehicle. During the secon week, estradiol-treated rats also received NA (0.12 or 1.0 mg/eat, sc, daily) or TAM (0.06 mg/rat) alone or in combination with NA (0.12mg). Serum prolactin levels were suppressed to the same extent in the TAM- and 1.0 mg NA-treated groups compared with rats given estrogen alone (2.3 ñ 0.3 and 5.6 ñ 1.5 ng/ml for TAM and NA groups vs 39.7 ñ 3.6 ng/ml for VE groups, P < 0.05). Except for the lowes dose of NA, uterine wet weight and DNA content were significant reduced in all groups compared to estradiol alone (236.8 ñ 18.0 and 295.6 ñ 27.8 mg vs 309.4 ñ 32.2 mg for uterine weight in TAM and NA groups vs VE, respectively, P 0.05; and 1.14 ñ 0.05 and 0.93 ñ 0.04 mg/uterus vs 1.33 ñ 0.06 mg/uterus for uterine DNA in TAM and NA groups vs VE groups). The combination of NA and TAM resulted in a higher degree of suppression of uterine growth than when each drug was used alone, indicating an additive antiproliferative effect of NA and TAM. Although no prolactin immunostaining was detected in the uterus of rats treated with estradiol, uterine immunoreactive prolactin was identified in those treated with NA, TAM ot both. These results suggest that an inhibitory effect on the action of estradiol can play a role in the hormonal modulation of uterine secretion