Estrogen potentiates adrenocortical responses to stress in female rats

2007 ◽  
Vol 292 (4) ◽  
pp. E1173-E1182 ◽  
Author(s):  
Helmer F. Figueiredo ◽  
Yvonne M. Ulrich-Lai ◽  
Dennis C. Choi ◽  
James P. Herman
Keyword(s):  
Mrna Expression ◽  
Acute Stress ◽  
Physiological Mechanism ◽  
Plasma Corticosterone ◽  
Female Rats ◽  
Inhibitory Effects ◽  
Ovx Rats ◽  
Glucocorticoid Response ◽  
Unexpected Findings ◽  
Adrenocortical Responses

It is well established that estrogens markedly enhance the glucocorticoid response to acute stress in females. However, the precise mechanism responsible for this regulation is poorly understood. Here, we tested whether estrogens enhance the activation of the paraventricular nucleus (PVN) of the hypothalamus by measuring stress-induced c- fos mRNA expression in the PVN of restraint-stressed ovariectomized (OVX) rats treated with physiologically relevant doses of estradiol (E2), the major female estrogen. As expected, E2 enhanced plasma corticosterone responses to restraint in OVX females. However, E2 markedly attenuated the stress-induced c- fos gene expression in the PVN and inhibited plasma ACTH responses in these animals. Furthermore, E2-inhibitory effects were mimicked by progesterone (P) alone or in combination with E2. Interestingly, the suppressive central effects of both E2 and P were apparently independent of basal paraventricular corticotropin-releasing hormone (CRH) transcription, since these ovarian steroids did not significantly affect PVN CRH mRNA expression in unstressed rats. These unexpected findings suggested that E2 promotes glucocorticoid hypersecretion in females by additional peripheral (i.e., adrenal) mechanisms. Indeed, E2 markedly enhanced plasma corticosterone responses and adrenal corticosterone content in dexamethasone-blocked OVX rats challenged with varying doses of exogenous ACTH. These results suggest that enhanced adrenal sensitive to ACTH is an important physiological mechanism mediating E2-related glucocorticoid hypersecretion in stressed females.

Stress- and cold-induced adrenocortical responses in repetitively immobilized or cold-acclimated rats

1987 ◽  
Vol 65 (7) ◽  
pp. 1448-1451 ◽  
Author(s):  
Takehiro Yahata ◽  
Kazuhiko Murazumi ◽  
Akihiro Kuroshima
Keyword(s):  
Cold Acclimation ◽  
Cold Exposure ◽  
Immobilization Stress ◽  
Acute Stress ◽  
Hormone Secretion ◽  
Plasma Corticosterone ◽  
Nonshivering Thermogenesis ◽  
Adrenocortical Hormone ◽  
Adrenocortical Responses

To evaluate the role of adrenocortical hormones in stress- or cold-induced nonshivering thermogenesis, plasma corticosterone (CS) and deoxycorticosterone (DOCS) were measured with the aid of HPLC under various conditions. Repetitive immobilization stress (3 h/day, for 1 or 4 weeks) elevated the resting level (24 h after the last immobilization) of CS, but not DOCS. Acute stress (immobilization for 30 min) or cold exposure (−5 °C for 15 min) caused marked increases of CS and DOCS in both nonstressed naive controls and repetitively stressed rats. Four weeks, but not 1 week, of repetitive immobilization stress potentiated the responsiveness of CS to both acute stress and cold, and that of DOCS to acute stress, but not to cold. Cold acclimation (5 °C, 4 weeks) significantly elevated both corticosteroids but did not affect the resting levels (18 h after being transferred to 25 °C) or the responsiveness of both CS and DOCS to either acute stress or cold. These results suggest that repetitive immobilization stress, but not cold acclimation, could enhance nonshivering thermogenesis, at least in part, through an improvement in the responsiveness of adrenocortical hormone secretion to acute stress or cold.

scholarly journals Intrahypothalamic Estradiol Modulates Hypothalamus-Pituitary-Adrenal-Axis Activity in Female Rats

Endocrinology ◽  
2012 ◽  
Vol 153 (7) ◽  
pp. 3337-3344 ◽  
Author(s):  
J. Liu ◽  
P. H. Bisschop ◽  
L. Eggels ◽  
E. Foppen ◽  
E. Fliers ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Restraint Stress ◽  
Acute Stress ◽  
Plasma Corticosterone ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Stress Exposure ◽  
Ici 182,780 ◽  
Hpa Axis Activity

Estrogen plays an important role in the regulation of the hypothalamus-pituitary-adrenal (HPA)-axis, but the neuroendocrine pathways and the role of estrogen receptor (ER) subtypes involved in specific aspects of this interaction remain unknown. In a first set of experiments, we administered estradiol (E2) intravenously, intracerebroventricularly, and by intrahypothalamic microdialysis to ovariectomized rats to measure plasma corticosterone (CORT) concentrations from carotid artery blood. Systemic infusion of E2 did not increase plasma CORT, but intracerebroventricular E2 induced a 3-fold CORT increase (P = 0.012). Local E2 infusions in the hypothalamic paraventricular nucleus (PVN) significantly increased plasma CORT (P < 0.001). A similar CORT increase was seen after PVN infusion of the ERα agonist propylpyrazoletriol, whereas the ERβ agonist diarylpropiolnitrile had no effect. In a second set of experiments, we investigated whether E2 modulates the HPA-axis response to acute stress by administering E2 agonists or its antagonist ICI 182,780 into the PVN during restraint stress exposure. After 30 min of stress exposure, plasma CORT had increased 5.0-fold (P < 0.001). E2 and propylpyrazoletriol administration in the PVN enhanced the stress-induced plasma CORT increase (8-fold vs. baseline), whereas ICI 182,780 and diarylpropiolnitrile reduced it, as compared with both E2 and vehicle administration in the PVN. In conclusion, central E2 modulates HPA-axis activity both in the basal state and during restraint stress. In the basal condition, the stimulation is mediated by ERα-sensitive neurons, whereas during stress, it is mediated by both ERα and ERβ.

Acute stress- or lipopolysaccharide-induced corticosterone secretion in female rats is independent of the oestrous cycle

1994 ◽  
Vol 131 (5) ◽  
pp. 535-539 ◽  
Author(s):  
Ai-Li Guo ◽  
Felice Petraglia ◽  
Mario Criscuolo ◽  
Guido Ficarra ◽  
Rossella E Nappi ◽  
...  
Keyword(s):  
Acute Stress ◽  
Plasma Corticosterone ◽  
Oestrous Cycle ◽  
Female Rats ◽  
Diurnal Changes ◽  
Experimental Conditions ◽  
Corticotrophin Releasing Factor ◽  
Swimming Stress ◽  
Corticosterone Secretion ◽  
Corticosterone Response

Guo A-L, Petraglia F, Criscuolo M, Ficarra G, Nappi RE, Palumbo M, Valentini A, Genazzani AR. Acute stress- or lipopolysaccharide-induced corticosterone secretion in female rats is independent of the oestrous cycle. Eur J Endocrinol 1994;131:535–9. ISSN 0804–4643 The aim of the present study was to test whether oestrous cycle is associated with the hypothalamus–pituitary–adrenal (HPA) axis function. Thus, corticosterone secretion in rats was investigated following lipopolysaccharide (LPS), acute cold-swimming or ether stress or synthetic corticotrophin-releasing factor (CRF) administration throughout the oestrous cycle. Moreover, plasma corticosterone response to cold-swimming stress or LPS administration also was studied at different times of day on pro-oestrus of di-oestrus-I. The following observations were obtained: the morning plasma corticosterone levels in control rats did not differ with the stage of the oestrous cycle; plasma corticosterone levels increased significantly following LPS administration (2 mg/kg, ip) or following acute exposure to cold (4°C)-swimming or ether stress. However, this increase in plasma corticosterone levels was not related to the stage of the oestrous cycle; synthetic CRF injection induced an increase in plasma corticosterone levels constant on di-oestrus-I and pro-oestrus; plasma corticosterone response to LPS administration or acute cold-swimming stress showed diurnal changes, with the lowest values at 18.00 h. which was independent of the oestrous cycle. By showing the unchanged corticosterone response to LPS, to acute stress and to exogenous CRF throughout the oestrous cycle, and the independence of the diurnal pattern of stress response on the oestrous cycle, the present study suggests that the oestrous cycle has no influence on the HPA activity under the present experimental conditions in rats. Andrea R Genazzani, Department of Obstetrics & Gynecology, University of Modena, Via del Pozzo 71, 41100 Modena, Italy

Dissociation of adrenal corticosteroid production from ACTH in water-restricted female rats

1981 ◽  
Vol 241 (1) ◽  
pp. R21-R24 ◽  
Author(s):  
R. G. Doell ◽  
M. F. Dallman ◽  
R. B. Clayton ◽  
G. D. Gray ◽  
S. Levine
Keyword(s):  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Female Rats ◽  
Adrenocorticotrophic Hormone ◽  
Corticosterone Concentration ◽  
Acth Concentration

These experiments were undertaken to investigate the mechanism whereby a precipitous drop in plasma corticosterone concentration is brought about following drinking in rats on a restricted water schedule. No alteration in adrenocorticotrophic hormone (ACTH) output was found, nor was catabolism of corticosterone sufficient to account for the drop. It is concluded that corticosterone level is controlled under these conditions by a mechanism independent of ACTH concentration.

scholarly journals Endothelin (ET)-1 and ET-3 inhibit estrogen and cAMP production by rat granulosa cells in vitro

1998 ◽  
Vol 157 (2) ◽  
pp. 209-215 ◽  
Author(s):  
AE Calogero ◽  
N Burrello ◽  
AM Ossino
Keyword(s):  
Granulosa Cells ◽  
Ovarian Function ◽  
Biological Effects ◽  
Female Rats ◽  
Dependent Manner ◽  
Camp Production ◽  
Inhibitory Effects ◽  
Ovarian Steroidogenesis ◽  
Estrogen Production ◽  
Etb Receptor

Endothelin (ET)-1 and ET-3, two peptides with a potent vasoconstrictive property, produce a variety of biological effects in different tissues by acting through two different receptors, the ET-1 selective ET(A) receptor and the non-selective ETB receptor. An increasing body of literature suggests that ET-1 acts as a paracrine/autocrine regulator of ovarian function. Indeed, ETB receptors have been identified in rat granulosa cells and ET-1 is a potent inhibitor of progesterone production. In contrast, inconsistent data have been reported about the role of ET-1 on estrogen production and the effects of ET-3 are not known. Therefore, the present study was undertaken to evaluate the effects of ET-1 and ET-3 on estrogen and cAMP production, and the receptor type involved. Given that prostanoids modulate ovarian steroidogenesis and that many actions of ETs are mediated by these compounds, we also evaluated whether the effects of ETs on estrogen and cAMP production might be prostanoid-mediated. ET-1, ET-3, and safarotoxin-S6c (SFX-S6c), a selective ETB receptor agonist, inhibited basal estrogen production by granulosa cells obtained from immature, estrogen-primed female rats, in a concentration-dependent manner. All three peptides were also capable of inhibiting the production of estrogen stimulated by a half-maximal (1 mIU/ml) and a maximally stimulatory (3 mIU/ml) concentration of FSH, ET-1 and ET-3 dose-dependently suppressed basal and FSH (1 mIU/ml)-stimulated cAMP production. ET-3 and SFX-S6c were significantly more potent than ET-1 in suppressing estrogen production, suggesting that this effect was not mediated by the ET(A) receptor. Indeed, BQ-123, a selective ET(A) receptor antagonist, did not influence the inhibitory effects of ET-1 and ET-3 on basal and FSH-stimulated estrogen release. To determine a possible involvement of prostanoids, we evaluated the effects of maximally effective concentrations of ET-1 and ET-3 on estrogen and cAMP production in the presence of indomethacin, a prostanoid synthesis inhibitor. This compound did not have any effect on the suppressive effects of ETs on basal or FSH (1 mIU/ml)-stimulated estrogen or cAMP production. In conclusion, ET-1 and ET-3 were able to inhibit estrogen and cAMP production by rat granulosa cells, indicating that the inhibitory effects of ETs on ovarian steroidogenesis are not limited to progesterone biosynthesis. This effect does not appear to be mediated by prostanoids or by the classical ET(A) and ETB receptors, at least under these experimental conditions.

scholarly journals Sex-specific vascular responses of the rat aorta: effects of moderate term (intermediate stage) streptozotocin-induced diabetes

2016 ◽  
Vol 94 (4) ◽  
pp. 408-415 ◽  
Author(s):  
Xiaoyuan Han ◽  
Sonali Shaligram ◽  
Rui Zhang ◽  
Leigh Anderson ◽  
Roshanak Rahimian
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mrna Expression ◽  
Intermediate Stage ◽  
Diabetic Rats ◽  
Female Rats ◽  
Diabetic Rat ◽  
Male And Female ◽  
Male And Female Rats ◽  
Oxide Synthase

Hyperglycemia affects male and female vascular beds differently. We have previously shown that 1 week after the induction of diabetes with streptozotocin (STZ), male and female rats exhibit differences in aortic endothelial function. To examine this phenomenon further, aortic responses were studied in male and female rats 8 weeks after the induction of diabetes (intermediate stage). Endothelium-dependent vasodilation (EDV) to acetylcholine (ACh) was measured in phenylephrine (PE) pre-contracted rat aortic rings. Concentration response curves to PE were generated before and after L-NAME, a nitric oxide synthase (NOS) inhibitor. Furthermore, mRNA expression of endothelial nitric oxide synthase (eNOS) and NADPH oxidase subunit (Nox1) were determined. At 8 weeks, diabetes impaired EDV to a greater extent in female than male aortae. Furthermore, the responsiveness to PE was significantly enhanced only in female diabetic rats, and basal NO, as indicated by the potentiation of the response to PE after L-NAME, was reduced in female diabetic rat aortae to the same levels as in males. In addition, eNOS mRNA expression was decreased, while the Nox1 expression was significantly enhanced in diabetic female rats. These results suggest that aortic function in female diabetic rats after 8 weeks exhibits a more prominent impairment and that NO may be involved.

Human placental lactogen inhibits growth without changing serum levels of IGF-1 in rats: an apparent specific action of the hormone

1992 ◽  
Vol 127 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Mimi H Chiang ◽  
Charles S Nicoll
Keyword(s):  
Epiphyseal Plate ◽  
Skeletal Growth ◽  
Female Rats ◽  
Placental Lactogen ◽  
Total Serum ◽  
Inhibitory Effects ◽  
Growth Inhibitory ◽  
Growth Promoting ◽  
Tibial Epiphyseal ◽  
Plate Width

Previous work in our laboratory has shown that the internal environment of rats has reduced growth-promoting activity during the second half of gestation and this condition is associated with resistance to the anabolic effects of GH. The placenta appears to be responsible for this condition but injections of estradiol plus progesterone into virgin females did not mimic it. Accordingly, it seemed worthwhile to test the effects of a placental lactogen (PL) for possible growth inhibitory effects. In the present study the effects of human (h)PL on skeletal growth in young female rats and on the growth of embryonic tissue transplants under their kidney capsules were investigated. Human (h) and bovine (b) GH, and ovine prolactin (oPRL) were also tested to determine whether the results obtained with hPL were specific. Twice daily subcutaneous injections of a high dose of hPL (10mg/day), but not of oPRL (5 mg/day) for 7 days inhibited both host tail growth and tibial epiphyseal plate width, and growth of whole 10-day embryo transplants. Injections of hGH at 1 mg/day for 8 days significantly increased host skeletal growth and growth of 12-day embryonic head transplants; at the same dose, neither bGH nor oPRL affected growth of the embryonic heads or of the host tibial epiphyseal plate width, but the bGH increased host tail growth. By contrast, the 1 mg/day dose of hPL significantly reduced the host's tibial epiphyseal plate width, tail growth, and transplant growth; lower doses of hPL (10 and 100 μg/day) were also inhibitory. Although all the hormone treatments increased total serum IGF-1 levels in the females, none of them had a significant effect when compared to saline injected control animals. Thus, the growth-inhibitory effects of hPL treatment appear to be specific to that hormone and they are not mediated by depression of serum IGF-1 levels. If these effects of hPL are mimicked by one or more of the rodent PLs, then the reduced growth-promoting activity and resistance to GH action that occurs in pregnant rats could be due to the rat PLs. These results indicate that in addition to having glucose-sparing effects in the mother, PLs could promote fetal growth by inhibiting growth of maternal tissues, which would thus spare other metabolites, such as amino acids and vitamins, for the conceptus.

Protective effects of estrogen on gender-specific development of diet-induced hypertension

2001 ◽  
Vol 91 (5) ◽  
pp. 2005-2009 ◽  
Author(s):  
Christian K. Roberts ◽  
Nosratola D. Vaziri ◽  
R. James Barnard
Keyword(s):  
Body Weight ◽  
Female Rats ◽  
Male Rats ◽  
Gonadal Hormone ◽  
Normal Female ◽  
Humoral Factors ◽  
Diet Modification ◽  
Ovx Rats ◽  
Hormone Status ◽  
Induced Hypertension

Dietary and humoral factors are thought to be involved in the development of hypertension. This study investigated the interaction between diet and gonadal hormone status in the development and reversibility of hypertension. Normal male and female and ovariectomized (OVX) female Fischer rats were placed on either a high-fat (primarily saturated), refined carbohydrate (sucrose) (HFS) or a low-fat, complex carbohydrate (LFCC) diet at 2 mo of age, and body weight and systolic blood pressure (BP) were measured. Male and OVX female rats were initially on the diets for 7 mo, whereas normal female rats were on the diets for 2 yr. After this initial phase, a group of rats from each of the normal HFS groups were converted to the LFCC diet for a period of 1 mo (males) and 2 mo (females). The OVX females were subcutaneously implanted with a 0.5-mg estradiol (E2) pellet for 1 mo. A significant rise in arterial BP occurred within 12 mo in female and only 2 mo in male rats on the HFS diet, exceeding 140 mmHg after 24 and 7 mo, respectively. Conversion from the HFS to the LFCC diet led to a normalization of BP in both female and male rats. HFS diet-induced hypertension was accelerated by OVX in female rats, approaching the pattern seen in male rats. The effect of OVX was completely reversed by E2replacement. BP did not significantly change in any of the LFCC groups at any time point, and E2 replacement had no effect on BP in the OVX LFCC group. All HFS groups had significantly greater body weight, with differences occurring sooner in the male and OVX rats compared with the female rats. Diet modification resulted in a partial but significant reduction of body weight, but E2replacement did not. These results demonstrate that long-term consumption of HFS diet induces hypertension in both genders and is reversible by diet modification. Hypertension is significantly delayed in females with functional ovaries. This protection is lost by OVX and restored by estrogen replacement. Thus hormone status contributes to the delayed onset of diet-induced hypertension in females compared with males.

Cardiac response to doxorubicin and dexrazoxane in intact and ovariectomized young female rats at rest and after swim training

2012 ◽  
Vol 302 (10) ◽  
pp. H2048-H2057 ◽  
Author(s):  
Annie Calvé ◽  
Rami Haddad ◽  
Sarah-Neiel Barama ◽  
Melissa Meilleur ◽  
Igal A. Sebag ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Adult Survivors ◽  
Young Female ◽  
Cardiac Response ◽  
Female Rats ◽  
Cancer Therapies ◽  
Sprague Dawley ◽  
Cardiac Damage ◽  
Ovx Rats ◽  
The Impact

The impact of cancer therapies on adult cardiac function is becoming a concern as more children survive their initial cancer. Cardiovascular disease is now a significant problem to adult survivors of childhood cancer. Specifically, doxorubicin (DOX) may be particularly harmful in young girls. The objective of this study was to characterize DOX damage and determine the ability of dexrazoxane (DEX) to reduce DOX-mediated cardiac damage in sedentary and swim-trained female rats. Female Sprague-Dawley rats were left intact or ovariectomized (OVX) at weaning then injected with DEX (60 mg/kg) before DOX (3 mg/kg), DOX alone, or PBS. Rats were separated into sedentary and swim cohorts. Body weight was reduced in DOX:DEX- but not PBS- or DOX-treated rats. Echocardiographic parameters were similar in sedentary rats. Swim training revealed greater concentric remodeling in DOX-treated rats and reduced fractional shortening in DOX:DEX-treated rats. Calsequestrin 2 was reduced with DOX and increased with DOX:DEX postswim. Sarco(endo)plasmic reticulum Ca2+-ATPase 2a was reduced and calsequestrin 2 reduced further by swim training only in intact rats. OVX rats were heavier and developed eccentric remodeling post-swim with DOX and eccentric hypertrophy with DOX:DEX. Changes in SERCA2a and calsequestrin 2 expression were not observed. Ovariectomized DOX- and DOX:DEX-treated rats stopped growing during swim training. DEX coinjection did not relieve DOX-mediated cardiotoxicity in intact or hormone-deficient rats. DOX-mediated reductions in growth, cardiac function, and expression of calcium homeostasis proteins were exacerbated by swim. DEX coadministration did not substantially relieve DOX-mediated cardiotoxicity in young female rats. Ovarian hormones reduce DOX-induced cardiotoxicity.

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