Hyperprolactinemia enhances ovarian estrogen responsiveness to gonadotropins in prepubertal rats: antagonistic effect of adrenalectomy.

J. P. Advis, L. I. Aguado, Sergio Ojeda

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Hyperprolactinemia (HP) induced in female rats by dopaminergic receptor blockers enhanced ovarian estradiol (E2) release in response to human chorionic gonadotropin (hCG) or human follicle-stimulating hormone (hFSH) in vitro. Uterine weight and ovarian aromatase activity were also increased. In contrast, ovarian androgen (A) release in response to hCG was reduced. Injections of ovine prolactin (oPrl) also enhanced E2 response to hCG in vitro. The increased E2 response was not due to a direct effect of Prl on ovarian aromatase activity since administration of oPrl to hypophysectomized rats failed to enhance the formation of E2 from testosterone (T) in vitro, and inhibited the increase in the enzyme activity induced by FSH. Adrenalectomy (ADRX) of intact rats, which did not affect mean serum gonadotropin levels, blunted the effect of HP on the E2 response to hCG. The suppression was partially reversed by corticosterone (B). Serum progesterone (P) and T were similar in controls and HP-ovariectomized (OVX) rats with intact adrenals. Likewise, serum androstenedione (delta 4) and dehydroepiandrosterone (DHA) were not altered in intact, HP rats as compared with controls. Thus, an increase in adrenal secretion of these steroids does not appear to mediate the effect of Prl on ovarian E2 response to gonadotropins. Ovaries of HP rats showed more large follicles than controls. In contrast, ovaries of HP-ADRX rats had a decreased number of large follicles. It is suggested that: a) in intact prepubertal rats Prl increases the E2 response of the ovary to gonadotropins by facilitating follicular development rather than by a direct action on aromatase activity, and b) when follicular development is stimulated by FSH, an inhibitory effect of Prl on aromatase activity becomes apparent. The effect of Prl on the E2 response of the ovary to gonadotropins is not mediated by the adrenal cortex. Rather, it appears that while Prl facilitates the development of large, E2-producing follicles by promoting the growth of small- and medium-sized follicles, an adrenal component influences follicular growth at a step subsequent to Prl.

Original languageEnglish (US)
Pages (from-to)181-194
Number of pages14
JournalBiology of Reproduction
Volume29
Issue number1
StatePublished - Aug 1983
Externally publishedYes

Fingerprint

Hyperprolactinemia
Adrenalectomy
Gonadotropins
Estrogens
Aromatase
Chorionic Gonadotropin
Ovary
Prolactin
Sheep
Serum
Human Follicle Stimulating Hormone
Dehydroepiandrosterone
Androstenedione
Adrenal Cortex
Growth
Corticosterone
Androgens
Progesterone
Testosterone
Estradiol

ASJC Scopus subject areas

  • Cell Biology
  • Developmental Biology
  • Embryology

Cite this

Hyperprolactinemia enhances ovarian estrogen responsiveness to gonadotropins in prepubertal rats : antagonistic effect of adrenalectomy. / Advis, J. P.; Aguado, L. I.; Ojeda, Sergio.

In: Biology of Reproduction, Vol. 29, No. 1, 08.1983, p. 181-194.

Research output: Contribution to journalArticle

@article{c61ee61fabbe46fd96468239ea51ef82,
title = "Hyperprolactinemia enhances ovarian estrogen responsiveness to gonadotropins in prepubertal rats: antagonistic effect of adrenalectomy.",
abstract = "Hyperprolactinemia (HP) induced in female rats by dopaminergic receptor blockers enhanced ovarian estradiol (E2) release in response to human chorionic gonadotropin (hCG) or human follicle-stimulating hormone (hFSH) in vitro. Uterine weight and ovarian aromatase activity were also increased. In contrast, ovarian androgen (A) release in response to hCG was reduced. Injections of ovine prolactin (oPrl) also enhanced E2 response to hCG in vitro. The increased E2 response was not due to a direct effect of Prl on ovarian aromatase activity since administration of oPrl to hypophysectomized rats failed to enhance the formation of E2 from testosterone (T) in vitro, and inhibited the increase in the enzyme activity induced by FSH. Adrenalectomy (ADRX) of intact rats, which did not affect mean serum gonadotropin levels, blunted the effect of HP on the E2 response to hCG. The suppression was partially reversed by corticosterone (B). Serum progesterone (P) and T were similar in controls and HP-ovariectomized (OVX) rats with intact adrenals. Likewise, serum androstenedione (delta 4) and dehydroepiandrosterone (DHA) were not altered in intact, HP rats as compared with controls. Thus, an increase in adrenal secretion of these steroids does not appear to mediate the effect of Prl on ovarian E2 response to gonadotropins. Ovaries of HP rats showed more large follicles than controls. In contrast, ovaries of HP-ADRX rats had a decreased number of large follicles. It is suggested that: a) in intact prepubertal rats Prl increases the E2 response of the ovary to gonadotropins by facilitating follicular development rather than by a direct action on aromatase activity, and b) when follicular development is stimulated by FSH, an inhibitory effect of Prl on aromatase activity becomes apparent. The effect of Prl on the E2 response of the ovary to gonadotropins is not mediated by the adrenal cortex. Rather, it appears that while Prl facilitates the development of large, E2-producing follicles by promoting the growth of small- and medium-sized follicles, an adrenal component influences follicular growth at a step subsequent to Prl.",
author = "Advis, {J. P.} and Aguado, {L. I.} and Sergio Ojeda",
year = "1983",
month = "8",
language = "English (US)",
volume = "29",
pages = "181--194",
journal = "Biology of Reproduction",
issn = "0006-3363",
publisher = "Society for the Study of Reproduction",
number = "1",

}

TY - JOUR

T1 - Hyperprolactinemia enhances ovarian estrogen responsiveness to gonadotropins in prepubertal rats

T2 - antagonistic effect of adrenalectomy.

AU - Advis, J. P.

AU - Aguado, L. I.

AU - Ojeda, Sergio

PY - 1983/8

Y1 - 1983/8

N2 - Hyperprolactinemia (HP) induced in female rats by dopaminergic receptor blockers enhanced ovarian estradiol (E2) release in response to human chorionic gonadotropin (hCG) or human follicle-stimulating hormone (hFSH) in vitro. Uterine weight and ovarian aromatase activity were also increased. In contrast, ovarian androgen (A) release in response to hCG was reduced. Injections of ovine prolactin (oPrl) also enhanced E2 response to hCG in vitro. The increased E2 response was not due to a direct effect of Prl on ovarian aromatase activity since administration of oPrl to hypophysectomized rats failed to enhance the formation of E2 from testosterone (T) in vitro, and inhibited the increase in the enzyme activity induced by FSH. Adrenalectomy (ADRX) of intact rats, which did not affect mean serum gonadotropin levels, blunted the effect of HP on the E2 response to hCG. The suppression was partially reversed by corticosterone (B). Serum progesterone (P) and T were similar in controls and HP-ovariectomized (OVX) rats with intact adrenals. Likewise, serum androstenedione (delta 4) and dehydroepiandrosterone (DHA) were not altered in intact, HP rats as compared with controls. Thus, an increase in adrenal secretion of these steroids does not appear to mediate the effect of Prl on ovarian E2 response to gonadotropins. Ovaries of HP rats showed more large follicles than controls. In contrast, ovaries of HP-ADRX rats had a decreased number of large follicles. It is suggested that: a) in intact prepubertal rats Prl increases the E2 response of the ovary to gonadotropins by facilitating follicular development rather than by a direct action on aromatase activity, and b) when follicular development is stimulated by FSH, an inhibitory effect of Prl on aromatase activity becomes apparent. The effect of Prl on the E2 response of the ovary to gonadotropins is not mediated by the adrenal cortex. Rather, it appears that while Prl facilitates the development of large, E2-producing follicles by promoting the growth of small- and medium-sized follicles, an adrenal component influences follicular growth at a step subsequent to Prl.

AB - Hyperprolactinemia (HP) induced in female rats by dopaminergic receptor blockers enhanced ovarian estradiol (E2) release in response to human chorionic gonadotropin (hCG) or human follicle-stimulating hormone (hFSH) in vitro. Uterine weight and ovarian aromatase activity were also increased. In contrast, ovarian androgen (A) release in response to hCG was reduced. Injections of ovine prolactin (oPrl) also enhanced E2 response to hCG in vitro. The increased E2 response was not due to a direct effect of Prl on ovarian aromatase activity since administration of oPrl to hypophysectomized rats failed to enhance the formation of E2 from testosterone (T) in vitro, and inhibited the increase in the enzyme activity induced by FSH. Adrenalectomy (ADRX) of intact rats, which did not affect mean serum gonadotropin levels, blunted the effect of HP on the E2 response to hCG. The suppression was partially reversed by corticosterone (B). Serum progesterone (P) and T were similar in controls and HP-ovariectomized (OVX) rats with intact adrenals. Likewise, serum androstenedione (delta 4) and dehydroepiandrosterone (DHA) were not altered in intact, HP rats as compared with controls. Thus, an increase in adrenal secretion of these steroids does not appear to mediate the effect of Prl on ovarian E2 response to gonadotropins. Ovaries of HP rats showed more large follicles than controls. In contrast, ovaries of HP-ADRX rats had a decreased number of large follicles. It is suggested that: a) in intact prepubertal rats Prl increases the E2 response of the ovary to gonadotropins by facilitating follicular development rather than by a direct action on aromatase activity, and b) when follicular development is stimulated by FSH, an inhibitory effect of Prl on aromatase activity becomes apparent. The effect of Prl on the E2 response of the ovary to gonadotropins is not mediated by the adrenal cortex. Rather, it appears that while Prl facilitates the development of large, E2-producing follicles by promoting the growth of small- and medium-sized follicles, an adrenal component influences follicular growth at a step subsequent to Prl.

UR - http://www.scopus.com/inward/record.url?scp=0020803209&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020803209&partnerID=8YFLogxK

M3 - Article

C2 - 6615964

AN - SCOPUS:0020803209

VL - 29

SP - 181

EP - 194

JO - Biology of Reproduction

JF - Biology of Reproduction

SN - 0006-3363

IS - 1

ER -