The infantile female rat: In vivo ovarian and adrenal steroidogenic responses to exogenous administration or to endogenously induced elevations of gonadotropins and ACTH

W. W. Andrews, M. Heiman, J. R. Porter, Sergio Ojeda

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

To investigate the role of luteinizing hormone (LH), follicle stimulating hormone (FSH) and adrenocorticotropic hormone (ACTH) in stimulating release of sex steroids from ovaries and/or adrenals of infantile female rats, serum estradiol (E2), progesterone (P), and androgens [testosterone + dihydrotestosterone (A)] were measured in ovariectomized (OVX) or adrenalectomized (ADX) 11-day-old female rats 1 h following a single i.v. injection of various doses of LH, FSH, or ACTH. Luteinizing hormone, but not FSH or ACTH, stimulated release of P and A from ovaries of ADX rats. Likewise, a single i.v. injection of LHRH (100 ng/100 g BW) given to elevate endogenous gonadotropin levels of ADX rats resulted in a significant increase in serum levels of ovarian P and A 90 min later. None of these treatments increased serum E2 levels of ADX rats. The release of E2 from the adrenal was stimulated only by ACTH. Surprisingly, the release of P and A from adrenals of OVX rats was stimulated by LH and FSH, as well as by ACTH. Subjecting the animals to various stressful stimuli to induce endogenous ACTH release resulted in a rise in serum levels of P and A from adrenals of OVX rats. However, an increase in endogenous serum gonadotropin levels induced by i.v. injection of LHRH or the i.v. administration of highly purified rat FSH failed to produce a significant elevation in levels of circulating P, A, or E, in OVX rats, suggesting that the effectiveness of the LH and FSH preparations initially used may have been due to ACTH contamination. Analysis of these NIH preparations by radioimmunoassay (RIA) or bioassay, using dispersed cortico-adrenal cells in culture, revealed the presence of small, but clearly measurable amounts of ACTH. Although the ACTH values obtained with RIA were distinctly higher than those measured by bioassay (RIA, 2000 pg/μg NIH-LH-B10 and 590 pg/μg NIH-FSH-S12; bioassay, 45 pg/μg LH and 98 pg/μg FSH), evaluation of the capability of these contaminating amounts to stimulate adrenal release of P and/or A following their in vitro or in vivo administration unambiguously indicated that the effect of both LH and FSH on the release of P and A from the adrenal was due to their ACTH contamination. Thus, in the infantile female rat, serum gonadotropins may significantly contribute to the maintenance of levels of circulating P and A via an ovarian but not an adrenal site of action. Additionally, ACTH may also participate in maintaining and/or altering the levels of circulating P, A, and, to a lesser extent, E2 via its stimulatory action on the infantile adrenal gland. Lastly the poor response to increases in both endogenous gonadotropin and ACTH levels in terms of E2 secretion and the persistence of measurable E2 after OVX and ADX suggest that the high serum E2 levels seen in infantile rats are more related to a prolonged half life (due to binding of alphafetoprotein) than to an enhanced secretory activity of the ovaries and adrenal glands.

Original languageEnglish (US)
Pages (from-to)597-608
Number of pages12
JournalBiology of Reproduction
Volume24
Issue number3
StatePublished - 1981
Externally publishedYes

Fingerprint

Gonadotropins
Adrenocorticotropic Hormone
Follicle Stimulating Hormone
Luteinizing Hormone
Serum
Biological Assay
Radioimmunoassay
Ovary
Adrenal Glands
Gonadotropin-Releasing Hormone
Injections
Dihydrotestosterone
Androgens
Progesterone
Half-Life
Testosterone
Estradiol
Cell Culture Techniques
Steroids
Maintenance

ASJC Scopus subject areas

  • Cell Biology
  • Developmental Biology
  • Embryology

Cite this

@article{8d20442f21214687b5146b43d110db5c,
title = "The infantile female rat: In vivo ovarian and adrenal steroidogenic responses to exogenous administration or to endogenously induced elevations of gonadotropins and ACTH",
abstract = "To investigate the role of luteinizing hormone (LH), follicle stimulating hormone (FSH) and adrenocorticotropic hormone (ACTH) in stimulating release of sex steroids from ovaries and/or adrenals of infantile female rats, serum estradiol (E2), progesterone (P), and androgens [testosterone + dihydrotestosterone (A)] were measured in ovariectomized (OVX) or adrenalectomized (ADX) 11-day-old female rats 1 h following a single i.v. injection of various doses of LH, FSH, or ACTH. Luteinizing hormone, but not FSH or ACTH, stimulated release of P and A from ovaries of ADX rats. Likewise, a single i.v. injection of LHRH (100 ng/100 g BW) given to elevate endogenous gonadotropin levels of ADX rats resulted in a significant increase in serum levels of ovarian P and A 90 min later. None of these treatments increased serum E2 levels of ADX rats. The release of E2 from the adrenal was stimulated only by ACTH. Surprisingly, the release of P and A from adrenals of OVX rats was stimulated by LH and FSH, as well as by ACTH. Subjecting the animals to various stressful stimuli to induce endogenous ACTH release resulted in a rise in serum levels of P and A from adrenals of OVX rats. However, an increase in endogenous serum gonadotropin levels induced by i.v. injection of LHRH or the i.v. administration of highly purified rat FSH failed to produce a significant elevation in levels of circulating P, A, or E, in OVX rats, suggesting that the effectiveness of the LH and FSH preparations initially used may have been due to ACTH contamination. Analysis of these NIH preparations by radioimmunoassay (RIA) or bioassay, using dispersed cortico-adrenal cells in culture, revealed the presence of small, but clearly measurable amounts of ACTH. Although the ACTH values obtained with RIA were distinctly higher than those measured by bioassay (RIA, 2000 pg/μg NIH-LH-B10 and 590 pg/μg NIH-FSH-S12; bioassay, 45 pg/μg LH and 98 pg/μg FSH), evaluation of the capability of these contaminating amounts to stimulate adrenal release of P and/or A following their in vitro or in vivo administration unambiguously indicated that the effect of both LH and FSH on the release of P and A from the adrenal was due to their ACTH contamination. Thus, in the infantile female rat, serum gonadotropins may significantly contribute to the maintenance of levels of circulating P and A via an ovarian but not an adrenal site of action. Additionally, ACTH may also participate in maintaining and/or altering the levels of circulating P, A, and, to a lesser extent, E2 via its stimulatory action on the infantile adrenal gland. Lastly the poor response to increases in both endogenous gonadotropin and ACTH levels in terms of E2 secretion and the persistence of measurable E2 after OVX and ADX suggest that the high serum E2 levels seen in infantile rats are more related to a prolonged half life (due to binding of alphafetoprotein) than to an enhanced secretory activity of the ovaries and adrenal glands.",
author = "Andrews, {W. W.} and M. Heiman and Porter, {J. R.} and Sergio Ojeda",
year = "1981",
language = "English (US)",
volume = "24",
pages = "597--608",
journal = "Biology of Reproduction",
issn = "0006-3363",
publisher = "Society for the Study of Reproduction",
number = "3",

}

TY - JOUR

T1 - The infantile female rat

T2 - In vivo ovarian and adrenal steroidogenic responses to exogenous administration or to endogenously induced elevations of gonadotropins and ACTH

AU - Andrews, W. W.

AU - Heiman, M.

AU - Porter, J. R.

AU - Ojeda, Sergio

PY - 1981

Y1 - 1981

N2 - To investigate the role of luteinizing hormone (LH), follicle stimulating hormone (FSH) and adrenocorticotropic hormone (ACTH) in stimulating release of sex steroids from ovaries and/or adrenals of infantile female rats, serum estradiol (E2), progesterone (P), and androgens [testosterone + dihydrotestosterone (A)] were measured in ovariectomized (OVX) or adrenalectomized (ADX) 11-day-old female rats 1 h following a single i.v. injection of various doses of LH, FSH, or ACTH. Luteinizing hormone, but not FSH or ACTH, stimulated release of P and A from ovaries of ADX rats. Likewise, a single i.v. injection of LHRH (100 ng/100 g BW) given to elevate endogenous gonadotropin levels of ADX rats resulted in a significant increase in serum levels of ovarian P and A 90 min later. None of these treatments increased serum E2 levels of ADX rats. The release of E2 from the adrenal was stimulated only by ACTH. Surprisingly, the release of P and A from adrenals of OVX rats was stimulated by LH and FSH, as well as by ACTH. Subjecting the animals to various stressful stimuli to induce endogenous ACTH release resulted in a rise in serum levels of P and A from adrenals of OVX rats. However, an increase in endogenous serum gonadotropin levels induced by i.v. injection of LHRH or the i.v. administration of highly purified rat FSH failed to produce a significant elevation in levels of circulating P, A, or E, in OVX rats, suggesting that the effectiveness of the LH and FSH preparations initially used may have been due to ACTH contamination. Analysis of these NIH preparations by radioimmunoassay (RIA) or bioassay, using dispersed cortico-adrenal cells in culture, revealed the presence of small, but clearly measurable amounts of ACTH. Although the ACTH values obtained with RIA were distinctly higher than those measured by bioassay (RIA, 2000 pg/μg NIH-LH-B10 and 590 pg/μg NIH-FSH-S12; bioassay, 45 pg/μg LH and 98 pg/μg FSH), evaluation of the capability of these contaminating amounts to stimulate adrenal release of P and/or A following their in vitro or in vivo administration unambiguously indicated that the effect of both LH and FSH on the release of P and A from the adrenal was due to their ACTH contamination. Thus, in the infantile female rat, serum gonadotropins may significantly contribute to the maintenance of levels of circulating P and A via an ovarian but not an adrenal site of action. Additionally, ACTH may also participate in maintaining and/or altering the levels of circulating P, A, and, to a lesser extent, E2 via its stimulatory action on the infantile adrenal gland. Lastly the poor response to increases in both endogenous gonadotropin and ACTH levels in terms of E2 secretion and the persistence of measurable E2 after OVX and ADX suggest that the high serum E2 levels seen in infantile rats are more related to a prolonged half life (due to binding of alphafetoprotein) than to an enhanced secretory activity of the ovaries and adrenal glands.

AB - To investigate the role of luteinizing hormone (LH), follicle stimulating hormone (FSH) and adrenocorticotropic hormone (ACTH) in stimulating release of sex steroids from ovaries and/or adrenals of infantile female rats, serum estradiol (E2), progesterone (P), and androgens [testosterone + dihydrotestosterone (A)] were measured in ovariectomized (OVX) or adrenalectomized (ADX) 11-day-old female rats 1 h following a single i.v. injection of various doses of LH, FSH, or ACTH. Luteinizing hormone, but not FSH or ACTH, stimulated release of P and A from ovaries of ADX rats. Likewise, a single i.v. injection of LHRH (100 ng/100 g BW) given to elevate endogenous gonadotropin levels of ADX rats resulted in a significant increase in serum levels of ovarian P and A 90 min later. None of these treatments increased serum E2 levels of ADX rats. The release of E2 from the adrenal was stimulated only by ACTH. Surprisingly, the release of P and A from adrenals of OVX rats was stimulated by LH and FSH, as well as by ACTH. Subjecting the animals to various stressful stimuli to induce endogenous ACTH release resulted in a rise in serum levels of P and A from adrenals of OVX rats. However, an increase in endogenous serum gonadotropin levels induced by i.v. injection of LHRH or the i.v. administration of highly purified rat FSH failed to produce a significant elevation in levels of circulating P, A, or E, in OVX rats, suggesting that the effectiveness of the LH and FSH preparations initially used may have been due to ACTH contamination. Analysis of these NIH preparations by radioimmunoassay (RIA) or bioassay, using dispersed cortico-adrenal cells in culture, revealed the presence of small, but clearly measurable amounts of ACTH. Although the ACTH values obtained with RIA were distinctly higher than those measured by bioassay (RIA, 2000 pg/μg NIH-LH-B10 and 590 pg/μg NIH-FSH-S12; bioassay, 45 pg/μg LH and 98 pg/μg FSH), evaluation of the capability of these contaminating amounts to stimulate adrenal release of P and/or A following their in vitro or in vivo administration unambiguously indicated that the effect of both LH and FSH on the release of P and A from the adrenal was due to their ACTH contamination. Thus, in the infantile female rat, serum gonadotropins may significantly contribute to the maintenance of levels of circulating P and A via an ovarian but not an adrenal site of action. Additionally, ACTH may also participate in maintaining and/or altering the levels of circulating P, A, and, to a lesser extent, E2 via its stimulatory action on the infantile adrenal gland. Lastly the poor response to increases in both endogenous gonadotropin and ACTH levels in terms of E2 secretion and the persistence of measurable E2 after OVX and ADX suggest that the high serum E2 levels seen in infantile rats are more related to a prolonged half life (due to binding of alphafetoprotein) than to an enhanced secretory activity of the ovaries and adrenal glands.

UR - http://www.scopus.com/inward/record.url?scp=0019490610&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0019490610&partnerID=8YFLogxK

M3 - Article

C2 - 6263376

AN - SCOPUS:0019490610

VL - 24

SP - 597

EP - 608

JO - Biology of Reproduction

JF - Biology of Reproduction

SN - 0006-3363

IS - 3

ER -