EFFECTS OF PROLACTIN ON PITUITARY-ADRENAL FUNCTION IN INTACT AND OVARIECTOMIZED RATS

1978 ◽  
Vol 88 (4) ◽  
pp. 744-753 ◽  
Author(s):  
Silvia B. Vasquez ◽  
Julian I. Kitay
Keyword(s):  
Reductase Activity ◽  
Combined Treatment ◽  
Plasma Corticosterone ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Response To Stress ◽  
Adrenal Response ◽  
Secretion Rates

ABSTRACT The influence of prolactin treatment (100 μg/100 g body wt. sc daily for 7 days) on plasma corticosterone levels, adrenal steroid production in vitro and in vivo and pituitary-adrenal responses to stress were studied in intact and castrated female rats. Prolactin enhanced plasma corticosterone levels and corticosterone production in vitro and in vivo in intact rats after stress. Differences were abolished with ACTH treatment. In contrast, prolactin administration to ovariectomized rats inhibited plasma corticosterone response to stress. Combined treatment with ACTH reversed these findings. A greater in vitro production of corticosterone by adrenal slices and adrenal homogenates associated with an effective inhibition of adrenal 5α-reductase activity were also observed. Secretion of DHB in adrenal venous blood was decreased as well, without changes in corticosterone or THB secretion rates. However, combined treatment with prolactin and ACTH produced greater increments in secretion rates of corticosterone than those obtained with prolactin alone. The data suggest that prolactin treatment to ovariectomized rats has a dual effect: a) adrenal responsiveness to ACTH is enhanced by its effects on adrenal 5α-reductase activity, and b) pituitary-adrenal response to stress is dampered by prolactin treatment. The effects of prolactin on adrenal 5α-reductase activity and corticosterone production in vitro were paralleled in vivo only after the exogenous administration of ACTH. The presence of the gonads apparently prevented the inhibitory effect of prolactin on ACTH secretion and in turn seemed to act synergistically with prolactin to facilitate pituitary-adrenal response to stress.

GONADOTROPHIN RELEASE IN VITRO, IN THE PRESENCE AND ABSENCE OF LUTEINIZING HORMONE RELEASING HORMONE, BY PITUITARY GLANDS FROM OVARIECTOMIZED AND SHAM-OPERATED IMMATURE FEMALE RATS OF VARIOUS AGES

1981 ◽  
Vol 88 (3) ◽  
pp. 375-379
Author(s):  
J. DULLAART
Keyword(s):  
Female Rats ◽  
Ovariectomized Rats ◽  
Immature Female ◽  
Releasing Hormone ◽  
Incubation Experiments ◽  
Immature Rats ◽  
Pituitary Glands ◽  
Lh Releasing Hormone

Hemipituitary glands of immature female rats, aged 10, 15, 20, 25, 30 and 35 days and either ovariectomized or sham-operated 5 days earlier, were incubated for 2 h in vitro with or without LH releasing hormone. Concentrations of LH and FSH were determined at the end of the incubations in the incubation media and in the hemipituitary glands, and also in the sera collected at the beginning of the incubation experiments. Results showed that in many instances gonadotrophin release was higher after incubation of glands of ovariectomized rats than with glands of control animals. However, these effects of ovariectomy were much smaller than those observed in vivo and were generally absent in rats of less than 20 days of age. It was concluded that ovariectomy may change the secretory characteristics of the gonadotrophic cells of immature rats but that such changes were largely restricted to immature rats older than 20 days.

EFFECTS OF TESTOSTERONE ON PITUITARY CORTICOTROPHIN AND ADRENAL STEROID SECRETION IN MALE AND FEMALE RATS

1963 ◽  
Vol 43 (4) ◽  
pp. 601-608 ◽  
Author(s):  
Julian I. Kitay
Keyword(s):  
Plasma Corticosterone ◽  
Female Rats ◽  
Male Rats ◽  
Intact Male ◽  
Male And Female ◽  
Adrenal Steroid ◽  
Adrenal Steroidogenesis ◽  
Male And Female Rats

ABSTRACT Administration of a depot testosterone preparation to male and female rats resulted in no change in body or pituitary weight in either sex. Pituitary corticotrophin content was unaltered in male animals but was reduced in females. Adrenal weights and adrenal RNA and DNA contents were decreased in both sexes. Plasma corticosterone concentrations were unaffected in males but were reduced in female rats after stress or corticotrophin injection. Hepatic reduction of ring A in vitro and biological half-life of corticosterone in vivo were unchanged in male animals but impaired in females. Testosterone administration to intact male rats significantly increased adrenal steroidogenesis measured in vitro. A significant decrease in steroid production was found in intact females but increased steroidogenesis was observed in adrenals from testosterone-treated oophorectomized animals. No effect was obtained following addition of testosterone directly in vitro. The data suggest that testosterone leads both to diminution of corticotrophin secretion and enhancement of adrenal steroid secretory capacity. In intact female rats, these effects are complicated by suppression of oestrogen secretion, the effects of which have been reported previously.

scholarly journals Biochemical effects of the porphyrinogenic drug allylisopropylacetamide. A comparative study with phenobarbital

1973 ◽  
Vol 134 (4) ◽  
pp. 859-868 ◽  
Author(s):  
Manchanahalli R. Satyanarayana Rao ◽  
Govindarajan Padmanaban
Keyword(s):  
Reductase Activity ◽  
Time Lag ◽  
Liver Weight ◽  
Microsomal Protein ◽  
Female Rats ◽  
Biochemical Effects ◽  
Increase Liver Weight ◽  
Cytochrome P 450

Successive administrations of allylisopropylacetamide, a potent porphyrinogenic drug, increase liver weight, microsomal protein and phospholipid contents. There is an increase in the rate of microsomal protein synthesis in vivo and in vitro. The drug decreases microsomal ribonuclease activity and increases NADPH–cytochrome c reductase activity. Phenobarbital, which has been reported to exhibit all these changes mentioned, is a weaker inducer of δ-aminolaevulinate synthetase and increases the rate of haem synthesis only after a considerable time-lag in fed female rats, when compared with the effects observed with allylisopropylacetamide. Again, phenobarbital does not share the property of allylisopropylacetamide in causing an initial decrease in cytochrome P-450 content. Haematin does not counteract most of the biochemical effects caused by allylisopropylacetamide, although it is quite effective in the case of phenobarbital. Haematin does not inhibit the uptake of [2-14C]allylisopropylacetamide by any of the liver subcellular fractions.

FAILURE TO INHIBIT CORTICOTROPHIN SECRETION BY EXPERIMENTALLY INDUCED INCREASES IN CORTICOID LEVELS

1963 ◽  
Vol 44 (1) ◽  
pp. 36-46 ◽  
Author(s):  
P. G. Smelik
Keyword(s):  
Acute Stress ◽  
Plasma Corticosterone ◽  
Blood Levels ◽  
Endogenous Production ◽  
Anaesthetized Rats ◽  
Response To Stress ◽  
Adrenal Response ◽  
Physiological Values ◽  
Physiological Variations

ABSTRACT The present experiments were designed in order to investigate whether physiological elevations in corticoid blood levels would inhibit the pituitary-adrenal response to stress. Plasma corticosterone (11β,21-dihydroxypregn-4-ene-3,20-dione) levels and the in vitro corticoid production by excised adrenals were determined in anaesthetized rats, pretreated with corticosterone solutions injected intravenously or intramuscularly. Intravenous administration of small amounts of corticosterone induced a very high but transient peak in plasma corticosterone concentrations. Corticosterone infusion caused a constant increase in plasma corticosterone levels. Increases exceeding maximal physiological values did not prevent the adrenocortical activation produced by histamine or corticotrophin. The summation of exogenous (infused) and endogenous (produced) corticosterone in the plasma became incomplete with increasing levels. This summation was not due to an increasing inhibition of the endogenous production, but to a higher rate of disappearance from the blood. It is concluded that these data are not in agreement with the »variable set point control theory[00AP], and demonstrate that physiological variations in plasma corticoid concentration do not affect the acute stress-induced corticotrophin release.

scholarly journals 17β-Estradiol, Aging, Inflammation, and the Stress Response in the Female Heart

Endocrinology ◽  
2011 ◽  
Vol 152 (4) ◽  
pp. 1589-1598 ◽  
Author(s):  
James P. Stice ◽  
Le Chen ◽  
Se-Chan Kim ◽  
J. S. Jung ◽  
A. L. Tran ◽  
...  
Keyword(s):  
Heat Shock ◽  
Cardiac Myocytes ◽  
Cytokine Expression ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
17Β Estradiol ◽  
Old Rats ◽  
Hypoxia Reoxygenation

Abstract Heat shock proteins (HSPs) are a cardioprotective class of proteins induced by stress and regulated by the transcription factor, heat shock factor (HSF)-1. 17β-estradiol (E2) indirectly regulates HSP expression through rapid activation of nuclear factor-κB (NF-κB) and HSF-1 and protects against hypoxia. As males experience a loss of protective cellular responses in aging, we hypothesized that aged menopausal (old ovariectomized) rats would have an impaired HSP response, which could be prevented by immediate in vivo E2 replacement. After measuring cardiac function in vivo, cardiac myocytes were isolated from ovariectomized adult and old rats with and without 9 weeks of E2 replacement. Myocytes were treated with E2in vitro and analyzed for activation of NF-κB, HSF-1, and HSP expression. In addition, we measured inflammatory cytokine expression and susceptibility to hypoxia/reoxygenation injury. Cardiac contractility was reduced in old ovariectomized rats and could prevented by immediate E2 replacement in vivo. Subsequent investigations in isolated cardiac myocytes found that in vitro E2 activated NF-κB, HSF-1, and increased HSP 72 expression in adult but not old rats. In response to hypoxia/reoxygenation, myocytes from adult, but not old, rats had increased HSP 72 expression. In addition, expression of the inflammatory cytokines TNF-α and IL-1β, as well as oxidative stress, were increased in myocytes from old ovariectomized rats; only the change in cytokine expression could be attenuated by in vivo E2 replacement. This study demonstrates that while aging in female rats led to a loss of the cardioprotective HSP response, E2 retains its protective cellular properties.

Stimulatory effect of caffeine on the hypothalamo-pituitary-adrenocortical axis in the rat

1989 ◽  
Vol 122 (2) ◽  
pp. 535-543 ◽  
Author(s):  
S. A. Nicholson
Keyword(s):  
Plasma Corticosterone ◽  
Corticotrophin Releasing Factor ◽  
Basal Release ◽  
Response To Stress ◽  
Corticosterone Response ◽  
Pharmacological Blockade ◽  
High Concentrations ◽  
Related Increase

ABSTRACT Intraperitoneal injection of caffeine (12·5–100 mg/kg) into rats caused a significant, dose-related increase in plasma corticosterone 2 h later, when the greatest response was measured. The corticosterone response to laparotomy stress or i.v. injection of ACTH(1–24) was unaffected by prior injection of caffeine. The response to stress or caffeine was unaffected by adrenal enucleation 28 days previously. In vitro, 10 mmol caffeine/l stimulated basal release of corticosterone from adrenal quarters and potentiated the response to a sub-maximal stimulatory concentration of cyclic AMP (cAMP). The drug had no effect on release stimulated by a sub-maximal concentration of ACTH(1–24). Release of ACTH from pituitary fragments incubated in vitro was stimulated in a dose-related manner by caffeine (0·01–10 mmol/l), and the responses to hypothalamic extract and sub-maximal concentrations of corticotrophin-releasing factor (CRF-41) or arginine vasopressin (AVP), but not cAMP, were significantly enhanced by 10 mmol caffeine/l. Release of immunoreactive CRF-41 (but not AVP) was significantly increased by caffeine (0·01–10 mmol/l) added to hypothalami incubated in vitro. The response to injection of caffeine in vivo was completely prevented by pharmacological blockade of endogenous CRF release. Taken together, these results show that caffeine at high concentrations can stimulate directly the release of the hormones of the hypothalamo-pituitary-adrenocortical axis in vitro, but the fact that these concentrations are unlikely to be reached after administration in vivo suggests that the effect of caffeine may be mediated centrally. Journal of Endocrinology (1989) 122, 535–543

scholarly journals Evidence for Ligand-Independent Activation of Hippocampal Estrogen Receptor-α by IGF-1 in Hippocampus of Ovariectomized Rats

Endocrinology ◽  
2016 ◽  
Vol 157 (8) ◽  
pp. 3149-3156 ◽  
Author(s):  
Elin M. Grissom ◽  
Jill M. Daniel
Keyword(s):  
Estrogen Receptor ◽  
Steroid Receptor ◽  
Estrogen Receptor Α ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Independent Manner ◽  
Steroid Receptor Coactivator ◽  
Intracerebroventricular Infusion

In the absence of ovarian estrogens, increased levels of estrogen receptor (ER)α in the hippocampus are associated with improvements in cognition. In vitro evidence indicates that under conditions of low estrogen, growth factors, including Insulin-Like Growth Factor 1 (IGF-1), can activate ERα and regulate ERα-mediated transcription through mechanisms that likely involve modification of phosphorylation sites on the receptor. The goal of the current work was to investigate a role for IGF-1 in ligand-independent activation of ERα in the hippocampus of female rats. Ovariectomized rats received a single intracerebroventricular infusion of IGF-1 and hippocampi were collected 1 or 24 hours later. After 1 h, IGF-1 increased hippocampal levels of phosphorylated ERα at serine 118 (S118) as revealed by Western blotting. Coimmunoprecipitation revealed that at 1 hour after infusion, IGF-1 increased association between ERα and steroid receptor coactivator 1, a histone acetyltransferase that increases transcriptional activity of phosphorylated ERα. IGF-1 infusion increased levels of the ERα-regulated proteins ERα, choline acetyltransferase, and brain-derived neurotrophic factor in the hippocampus 24 hours after infusion. Results indicate that IGF-1 activates ERα in ligand-independent manner in the hippocampus via phosphorylation at S118 resulting in increased association of ERα with steroid receptor coactivator 1 and elevation of ER-regulated proteins. To our knowledge, these data are the first in vivo evidence of ligand-independent actions of ERα and provide a mechanism by which ERα can impact memory in the absence of ovarian estrogens.

Excess in vitro prolactin secretion by pituitary cells from ovariectomized old rats

1984 ◽  
Vol 247 (4) ◽  
pp. E483-E488
Author(s):  
M. Haji ◽  
G. S. Roth ◽  
M. R. Blackman
Keyword(s):  
In Vitro Release ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Pituitary Cells ◽  
Lh Release ◽  
Old Rats

Various in vivo and in vitro pituitary lactotropic and gonadotropic functions were measured in mature (6-7 mo, normally cycling) and old (24 mo, constant diestrus) female Wistar rats. Serum prolactin (PRL) levels were higher (P less than 0.001), whereas luteinizing hormone (LH) values were similar (P greater than 0.05) in old versus mature rats both before and 3 days after ovariectomy. Serum PRL levels decreased significantly (P less than 0.005) postovariectomy only in the mature rats. The in vitro release of PRL and LH was measured for 4 days in primary adenohypophyseal cell cultures from the ovariectomized rats. Both basal and 17 beta-estradiol (E2)-stimulated PRL release (P less than 0.001) and production (P less than 0.005) were greater by cells from old rats. In contrast, both basal release and E2-stimulated LH release were greater (P less than 0.001) by cells from mature rats. Peak PRL release by cells from both old and mature rats occurred after exposure to E2 doses 1/100th of those required for peak LH release. These data support the hypothesis that intrinsic derangements in anterior pituitary function contribute to the reproductive decline in aging female rats and that different pituitary cell types exhibit discordant age changes in estrogenic sensitivity.

Autonomous FSH synthesis in vitro in anterior pituitary glands and grafts from female rats

1991 ◽  
Vol 129 (1) ◽  
pp. 27-33 ◽  
Author(s):  
J. A. M. J. van Dieten ◽  
J. de Koning ◽  
G. P. van Rees
Keyword(s):  
Follicular Fluid ◽  
Anterior Pituitary ◽  
Female Rats ◽  
Regulatory Mechanisms ◽  
Ovariectomized Rats ◽  
Intact Female ◽  
Pituitary Glands

ABSTRACT When pituitary glands from intact female, but not from ovariectomized rats, are incubated for 8 h in medium TC199 without further additives, FSH is synthesized. This LHRH-independent (or autonomous) FSH synthesis is prevented when bovine follicular fluid (bFF) is added to the incubation medium. Results from preliminary experiments, however, indicate no clear autonomous FSH synthesis after long-term absence of LHRH. To investigate the regulatory mechanisms involved in autonomous FSH synthesis and release, pituitary glands (exposed to endogenous LHRH) and pituitary grafts (not exposed to endogenous LHRH) from intact and ovariectomized rats were incubated for 8 h in medium TC199. Total FSH content (FSH released plus FSH remaining in the tissue) was compared with that in non-incubated glands or grafts, giving an indication of FSH synthesis. In addition, some of the animals were given LHRH pulses for 40 h before incubation. When pituitary tissue was taken from intact female rats, FSH synthesis occurred in the animals' own glands and in grafts from LHRH-pretreated rats. No FSH synthesis was seen in ovariectomized rats with or without pretreatment with bFF and/or LHRH. However, when ovariectomized rats had been pretreated with oestrogen, FSH synthesis was measured in vitro after pulsatile LHRH treatment in vivo. The results indicate that autonomous FSH synthesis in vitro is dependent upon previous (in vivo) exposure of the glands to both oestrogen and LHRH. Journal of Endocrinology (1991) 129, 27–33

MiR-22/Sp-1 Links Estrogens With the Up-Regulation of Cystathionine γ-Lyase in Myocardium, Which Contributes to Estrogenic Cardioprotection Against Oxidative Stress

Endocrinology ◽  
2015 ◽  
Vol 156 (6) ◽  
pp. 2124-2137 ◽  
Author(s):  
Long Wang ◽  
Zhi-Ping Tang ◽  
Wei Zhao ◽  
Bing-Hai Cong ◽  
Jian-Qiang Lu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Estrogen Receptor ◽  
Critical Role ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Receptor Subtypes ◽  
Down Regulation ◽  
Neonatal Cardiomyocytes

Abstract Hydrogen sulfide, generated in the myocardium predominantly via cystathionine-γ-lyase (CSE), is cardioprotective. Our previous study has shown that estrogens enhance CSE expression in myocardium of female rats. The present study aims to explore the mechanisms by which estrogens regulate CSE expression, in particular to clarify the role of estrogen receptor subtypes and the transcriptional factor responsible for the estrogenic effects. We found that either the CSE inhibitor or the CSE small interfering RNA attenuated the protective effect of 17β-estradiol (E2) against H2O2- and hypoxia/reoxygenation-induced injury in primary cultured neonatal cardiomyocytes. E2 stimulates CSE expression via estrogen receptor (ER)-α both in cultured cardiomyocytes in vitro and in the myocardium of female mice in vivo. A specificity protein-1 (Sp-1) consensus site was identified in the rat CSE promoter and was found to mediate the E2-induced CSE expression. E2 increases ERα and Sp-1 and inhibits microRNA (miR)-22 expression in myocardium of ovariectomized rats. In primary cardiomyocytes, E2 stimulates Sp-1 expression through the ERα-mediated down-regulation of miR-22. It was confirmed that both ERα and Sp-1 were targeted by miR-22. In the myocardium of ovariectomized rats, the level of miR-22 inversely correlated to CSE, ERα, Sp-1, and antioxidant biomarkers and positively correlated to oxidative biomarkers. In summary, this study demonstrates that estrogens stimulate Sp-1 through the ERα-mediated down-regulation of miR-22 in cardiomyocytes, leading to the up-regulation of CSE, which in turn results in an increase of antioxidative defense. Interaction of ERα, miR-22, and Sp-1 may play a critical role in the control of oxidative stress status in the myocardium of female rats.

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