17β-Estradiol modulates baroreflex sensitivity and autonomic tone of female rats

Female mammals have an enhanced baroreflex sensitivity compared with their male counterparts, leading researchers to speculate that estrogen modulates autonomic tone. Therefore, this study tests the hypothesis that exogenous estrogen can enhance the baroreflex sensitivity of male rats. Male Sprague-Dawley rats anesthetized with thiobutabarbitol sodium (50 mg/kg) were instrumented to measure blood pressure and heart rate and for the intravenous injection of drugs. The baroreflex was tested using intravenous injections of phenylephrine (0.025, 0.05, and 0.1 mg/kg), and the cardiovascular responses were plotted to obtain a measure of the sensitivity of the cardiac baroreflex. Intravenous injection of estrogen produced dose-related increases in the baroreflex sensitivity due to an increase in the magnitude of the reflex bradycardia. In a separate group of animals, stimulation of the vagus nerve for 2 h resulted in a decrease in baroreflex sensitivity. This effect was blocked when estrogen (1 × 10−2 mg/kg) was administered immediately before the end of stimulation. In conclusion, intravenous injection of estrogen in male rats significantly enhanced baroreflex sensitivity and blocked the attenuation in the baroreflex sensitivity observed after vagal stimulation.

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Regulation of components of the brain and cardiac renin-angiotensin systems by 17β-estradiol after myocardial infarction in female rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00497.2005 ◽

2006 ◽

Vol 291 (1) ◽

pp. R155-R162 ◽

Cited By ~ 9

Author(s):

Stephanie A. Dean ◽

Junhui Tan ◽

Roselyn White ◽

Edward R. O’Brien ◽

Frans H. H. Leenen

Keyword(s):

Myocardial Infarction ◽

Left Ventricular ◽

Female Rats ◽

Lv Function ◽

Coronary Artery Ligation ◽

Brain Nuclei ◽

Renin Angiotensin ◽

Lv Dysfunction ◽

17Β Estradiol ◽

The Brain

The present study tested the hypothesis that 17β-estradiol (E2) inhibits increases in angiotensin-converting enzyme (ACE) and ANG II type 1 receptor (AT1R) in the brain and heart after myocardial infarction (MI) and, thereby, inhibits development of left ventricular (LV) dysfunction after MI. Age-matched female Wistar rats were treated as follows: 1) no surgery (ovary intact), 2) ovariectomy + subcutaneous vehicle treatment (OVX + Veh), or 3) OVX + subcutaneous administration of a high dose of E2 (OVX + high-E2). After 2 wk, rats were randomly assigned to coronary artery ligation (MI) and sham operation groups and studied after 3 wk. E2 status did not affect LV function in sham rats. At 2–3 wk after MI, impairment of LV function was similar across MI groups, as measured by echocardiography and direct LV catheterization. LV ACE mRNA abundance and activity were increased severalfold in all MI groups compared with respective sham animals and to similar levels across MI groups. In most brain nuclei, ACE and AT1R densities increased after MI. Unexpectedly, compared with the respective sham groups the relative increase was clearest (20–40%) in OVX + high-E2 MI rats, somewhat less (10–15%) in ovary-intact MI rats, and least (<10–15%) in OVX + Veh MI rats. However, because in the sham group brain ACE and AT1R densities increased in the OVX + Veh rats and decreased in the OVX + high-E2 rats compared with the ovary-intact rats, actual ACE and AT1R densities in most brain nuclei were modestly higher (<20%) in OVX + Veh MI rats than in the other two MI groups. Thus E2 does not inhibit upregulation of ACE in the LV after MI and amplifies the percent increases in ACE and AT1R densities in brain nuclei after MI, despite E2-induced downregulation in sham rats. Consistent with these minor variations in the tissue renin-angiotensin system, during the initial post-MI phase, E2 appears not to enhance or hinder the development of LV dysfunction.

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Salvia officinalis Extract and 17β-Estradiol Suppresses Ovariectomy Induced Osteoporosis in Female Rats

Pakistan Journal of Biological Sciences ◽

10.3923/pjbs.2021.434.444 ◽

2021 ◽

Vol 24 (3) ◽

pp. 434-444

Author(s):

Bosy Azmy Abd E ◽

Marwa Tarek Ebra ◽

Hanaa Khairy Moh

Keyword(s):

Salvia Officinalis ◽

Female Rats ◽

17Β Estradiol

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Abstract 237: Sex-specific Regulation Of Collagen I And III Expression By 17β-estradiol In Rat Cardiac Fibroblasts: Role Of Estrogen Receptors

Circulation Research ◽

10.1161/res.113.suppl_1.a237 ◽

2013 ◽

Vol 113 (suppl_1) ◽

Author(s):

Elke Dworatzek ◽

Shokoufeh Mahmoodzadeh ◽

Sandra Kunze ◽

Vera Regitz-Zagrosek

Keyword(s):

Sex Differences ◽

Western Blot ◽

Estrogen Receptors ◽

Cardiac Fibrosis ◽

Cardiac Fibroblasts ◽

Collagen I ◽

Female Rats ◽

17Β Estradiol ◽

Specific Regulation

Clinical and animal studies showed in female pressure-overloaded hearts less cardiac fibrosis and collagen I and III gene expression compared to males, suggesting an inhibitory effect of 17β-Estradiol (E2) on collagens. Therefore we investigated the role of E2 and estrogen receptors (ER) on collagen I and III expression in isolated rat cardiac fibroblasts from both sexes. Cardiac fibroblasts were isolated from adult male and female Wistar rats, and treated with E2 (10-8M), vehicle, ERα and ERβ-agonist (10-7M) and/or pre-treated with ICI 182,780 (10-5M) for 24h. Cellular localization of ER in cardiac fibroblasts with/without E2 was detected by immunofluorescence staining, and expression of both ER was determined by western blot. Expression of collagen I and III was determined by qRT-PCR and western blot. E2-treatment led to a nuclear translocation of ERα and ERβ in cardiac fibroblasts, suggesting the functional activity of ER as transcription factors. Furthermore in cardiac fibroblasts from female rats E2 led to a significant down-regulation of collagen I and III gene and protein expression. In contrast there was a significant increase of collagen I and III levels in fibroblasts isolated from male rat hearts by E2. E2-effect could be inhibited by ICI 182, 780 indicating the involvement of ER. In cardiac fibroblasts from female rats, ERα-agonist treatment led to a significant down-regulation of collagen I and III mRNA level, but ERβ-agonist had no effects. In contrast, ERβ-agonist treatment of cardiac fibroblasts from males increased collagen I and III mRNA, but no changes with ERα agonist-treatment were detected. ERα protein levels displayed no sex differences at basal level. After E2-treatment ERα protein was up-regulated in male cells, but decreased in cardiac fibroblasts from females. ERβ protein was higher in female cells compared to males, but the expression was not regulated by E2 in both sexes. Sex-specific regulation of collagen I and III expression by E2 in cardiac fibroblasts might be responsible for sex-differences in cardiac fibrosis. This might be due to sexually dimorphic ER expression and regulation. Understanding how E2 and ER mediate sex-differences in cardiac remodeling may help to design sex-specific pharmacological interventions.

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Effects of ovariectomy and estrogen on ischemia-reperfusion injury in hindlimbs of female rats

Journal of Applied Physiology ◽

10.1152/jappl.2001.91.4.1828 ◽

2001 ◽

Vol 91 (4) ◽

pp. 1828-1835 ◽

Cited By ~ 60

Author(s):

Nicole Stupka ◽

Peter M. Tiidus

Keyword(s):

Muscle Damage ◽

Ischemia Reperfusion Injury ◽

Serum Insulin ◽

Ischemia Reperfusion ◽

Neutrophil Infiltration ◽

Female Rats ◽

Protective Effects ◽

Sprague Dawley ◽

Sprague Dawley Rats ◽

17Β Estradiol

The effects of estrogen and ovariectomy on indexes of muscle damage after 2 h of complete hindlimb ischemia and 2 h of reperfusion were investigated in female Sprague-Dawley rats. The rats were assigned to one of three experimental groups: ovariectomized with a 17β-estradiol pellet implant (OE), ovariectomized with a placebo pellet implant (OP), or control with intact ovaries (R). It was hypothesized that following ischemia-reperfusion (I/R), muscle damage indexes [serum creatine kinase (CK) activity, calpain-like activity, inflammatory cell infiltration, and markers of lipid peroxidation (thiobarbituric-reactive substances)] would be lower in the OE and R rats compared with the OP rats due to the protective effects of estrogen. Serum CK activity following I/R was greater ( P < 0.01) in the R rats vs. OP rats and similar in the OP and OE rats. Calpain-like activity was greatest in the R rats ( P < 0.01) and similar in the OP and OE rats. Neutrophil infiltration was assessed using the myeloperoxidase (MPO) assay and immunohistochemical staining for CD43-positive (CD43+) cells. MPO activity was lower ( P < 0.05) in the OE rats compared with any other group and similar in the OP and R rats. The number of CD43+ cells was greater ( P < 0.01) in the OP rats compared with the OE and R rats and similar in the OE and R rats. The OE rats had lower ( P < 0.05) thiobarbituric-reactive substance content following I/R compared with the R and OP rats. Indexes of muscle damage were consistently attenuated in the OE rats but not in the R rats. A 10-fold difference in serum estrogen content may mediate this. Surprisingly, serum CK activity and muscle calpain-like activity were lower ( P< 0.05) in the OP rats compared with the R rats. Increases in serum insulin-like growth factor-1 content ( P < 0.05) due to ovariectomy were hypothesized to account for this finding. Thus both ovariectomy and estrogen supplementation have differential effects on indexes of I/R muscle damage.

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17β-Estradiol attenuates blood–brain barrier disruption induced by cerebral ischemia–reperfusion injury in female rats

Brain Research ◽

10.1016/j.brainres.2005.08.048 ◽

2005 ◽

Vol 1060 (1-2) ◽

pp. 55-61 ◽

Cited By ~ 74

Author(s):

Ran Liu ◽

Yi Wen ◽

Evelyn Perez ◽

Xiaofei Wang ◽

Arthur L. Day ◽

...

Keyword(s):

Cerebral Ischemia ◽

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Female Rats ◽

Blood Brain Barrier Disruption ◽

Cerebral Ischemia Reperfusion ◽

Cerebral Ischemia Reperfusion Injury ◽

17Β Estradiol ◽

Brain Barrier Disruption

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Risk-based Decision Making in Rats: Modulation by Sex and Amphetamine

10.1101/2020.03.09.981563 ◽

2020 ◽

Author(s):

Dannia Islas-Preciado ◽

Steven R. Wainwright ◽

Julia Sniegocki ◽

Stephane E. Lieblich ◽

Shunya Yagi ◽

...

Keyword(s):

Decision Making ◽

Sex Differences ◽

Gonadal Hormones ◽

Risky Choice ◽

Female Rats ◽

Male Rats ◽

Risky Decision Making ◽

Risky Decision ◽

17Β Estradiol ◽

Males And Females

AbstractDecision-making is a complex process essential to daily adaptation in many species. Risk is an inherent aspect of decision-making and it is influenced by gonadal hormones. Testosterone and 17β-estradiol may modulate decision making and impact the mesocorticolimbic dopamine pathway. Here, we explored sex differences, the effect of gonadal hormones and the dopamine agonist amphetamine on risk-based decision making. Intact or gonadectomised (GDX) male and female rats underwent to a probabilistic discounting task. High and low doses of testosterone propionate (1.0 or 0.2 mg) and 17β-estradiol benzoate (0.3 μg) were administered to assess acute effects on risk-based decision making. After 3-days of washout period, intact and GDX rats received high or low (0.5 or 0.125 mg/kg) doses of amphetamine and re-tested in the probabilistic discounting task. Under baseline conditions, males made more risky choices during probability discounting compared to female rats, particularly in the lower probability blocks, but GDX did not influence risky choice. The high, but not the low dose, of testosterone modestly reduced risky decision making in GDX male rats. Conversely, 17β-estradiol had no significant effect on risky choice regardless of GDX status in either sex. Lastly, a higher dose of amphetamine increased risky decision making in both intact males and females, but had no effect in GDX rats. These findings demonstrated sex differences in risk-based decision making, with males showing a stronger bias towards larger, uncertain rewards. GDX status influenced the effects of amphetamine, suggesting different dopaminergic regulation in risk-based choices among males and females.

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