scholarly journals Stress, rejection, and hormones: Cortisol and progesterone reactivity to laboratory speech and rejection tasks in women and men

F1000Research ◽  
2014 ◽  
Vol 3 ◽  
pp. 208 ◽  
Author(s):  
Allison E. Gaffey ◽  
Michelle M. Wirth
Keyword(s):  
Hpa Axis ◽  
Social Rejection ◽  
Laboratory Setting ◽  
Hormonal Responses ◽  
Hypothalamic Pituitary Adrenal ◽  
The Social ◽  
Speech Control ◽  
Future Work ◽  
Hpa Axis Activity ◽  
Expected Increase

Stress and social rejection have important impacts on health. Among the mechanisms implicated are hormonal systems such as the hypothalamic-pituitary-adrenal (HPA) axis, which produces cortisol in humans. Current research employs speech stressors and social rejection stressors to understand hormonal responses in a laboratory setting. However, it is not clear whether social rejection stressors elicit hormonal reactivity. In addition to cortisol, progesterone has been highlighted as a potential stress- and affiliation-related hormone in humans. In the present study, 131 participants (70 men and 61 women) were randomly assigned to be exposed to one of four conditions: standardized speech stressor; speech control; social rejection task; or a control (inclusion) version of the social rejection task. Saliva samples were collected throughout the study to measure cortisol and progesterone. As hypothesized, we found the expected increase in cortisol in the speech stressor, and we also found that the social rejection task did not increase cortisol, underscoring the divergence between unpleasant experiences and HPA axis activity. However, we did not find evidence for progesterone increase either during the speech- or social rejection tasks. Compared with past studies on progesterone and stress in humans, the present findings present a mixed picture. Future work is needed to delineate the contexts and types of manipulations which lead to progesterone increases in humans.

scholarly journals Stress, rejection, and hormones: Cortisol and progesterone reactivity to laboratory speech and rejection tasks in women and men

F1000Research ◽  
2014 ◽  
Vol 3 ◽  
pp. 208 ◽  
Author(s):  
Allison E. Gaffey ◽  
Michelle M. Wirth
Keyword(s):  
Hpa Axis ◽  
Social Rejection ◽  
Laboratory Setting ◽  
Hormonal Responses ◽  
Hypothalamic Pituitary Adrenal ◽  
The Social ◽  
Speech Control ◽  
Future Work ◽  
Hpa Axis Activity ◽  
Expected Increase

Stress and social rejection have important impacts on health. Among the mechanisms implicated are hormonal systems such as the hypothalamic-pituitary-adrenal (HPA) axis, which produces cortisol in humans. Current research employs speech stressors and social rejection stressors to understand hormonal responses in a laboratory setting. However, it is not clear whether social rejection stressors elicit hormonal reactivity. In addition to cortisol, progesterone has been highlighted as a potential stress- and affiliation-related hormone in humans. In the present study, 131 participants (70 men and 61 women) were randomly assigned to be exposed to one of four conditions: standardized speech stressor; speech control; social rejection task; or a control (inclusion) version of the social rejection task. Saliva samples were collected throughout the study to measure cortisol and progesterone. As hypothesized, we found the expected increase in cortisol in the speech stressor, and we also found that the social rejection task did not increase cortisol, underscoring the divergence between unpleasant experiences and HPA axis activity. However, we did not find evidence for progesterone increase either during the speech- or social rejection tasks. Compared with past studies on progesterone and stress in humans, the present findings present a mixed picture. Future work is needed to delineate the contexts and types of manipulations which lead to progesterone increases in humans.

Effects of alprazolam on cholecystokinin-tetrapeptide (CCK-4) induced panic and hypothalamic-pituitary-adrenal (HPA) axis activity

2004 ◽  
Vol 36 (05) ◽  
Author(s):  
D Eser ◽  
P Zwanzger ◽  
S Aicher ◽  
C Schüle ◽  
TC Baghai ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Hypothalamic Pituitary Adrenal ◽  
Hpa Axis Activity

scholarly journals Vitamin A regulates hypothalamic–pituitary–adrenal axis status in LOU/C rats

2013 ◽  
Vol 219 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Nathalie Marissal-Arvy ◽  
Rachel Hamiani ◽  
Emmanuel Richard ◽  
Marie-Pierre Moisan ◽  
Véronique Pallet
Keyword(s):  
Vitamin A ◽  
Hpa Axis ◽  
Restraint Stress ◽  
Vitamin A Deficiency ◽  
Plasma Corticosterone ◽  
Hypothalamic Pituitary Adrenal ◽  
Corticosteroid Receptors ◽  
Vitamin A Status ◽  
Corticosterone Response ◽  
Hpa Axis Activity

The aim of this study was to explore the involvement of retinoids in the hypoactivity and hyporeactivity to stress of the hypothalamic–pituitary–adrenal (HPA) axis in LOU/C rats. We measured the effects of vitamin A deficiency administered or not with retinoic acid (RA) on plasma corticosterone in standard conditions and in response to restraint stress and on hypothalamic and hippocampal expression of corticosteroid receptors, corticotropin-releasing hormone and 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) in LOU/C rats. Interestingly, under control conditions, we measured a higher plasma concentration of retinol in LOU/C than in Wistar rats, which could contribute to the lower basal activity of the HPA axis in LOU/C rats. Vitamin A deficiency induced an increased HPA axis activity in LOU/C rats, normalized by RA administration. Compared with LOU/C control rats, vitamin A-deficient rats showed a delayed and heightened corticosterone response to restraint stress. The expression of corticosteroid receptors was strongly decreased by vitamin A deficiency in the hippocampus, which could contribute to a less efficient feedback by corticosterone on HPA axis tone. The expression of 11β-HSD1 was increased by vitamin A deficiency in the hypothalamus (+62.5%) as in the hippocampus (+104.7%), which could lead to a higher production of corticosterone locally and contribute to alteration of the hippocampus. RA supplementation treatment restored corticosterone concentrations and 11β-HSD1 expression to control levels. The high vitamin A status of LOU/C rats could contribute to their low HPA axis activity/reactivity and to a protective effect against 11β-HSD1-mediated deleterious action on cognitive performances during ageing.

Effects of prolonged exendin-4 administration on hypothalamic-pituitary-adrenal axis activity and water balance

2013 ◽  
Vol 304 (10) ◽  
pp. E1105-E1117 ◽  
Author(s):  
Manuel Gil-Lozano ◽  
Marina Romaní-Pérez ◽  
Verónica Outeiriño-Iglesias ◽  
Eva Vigo ◽  
Patricia L. Brubaker ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Hpa Axis ◽  
Stress Responses ◽  
Fold Increase ◽  
Acute Administration ◽  
Sprague Dawley ◽  
Hypothalamic Pituitary Adrenal ◽  
Sprague Dawley Rats ◽  
Glucagon Like Peptide 1 ◽  
Hpa Axis Activity

Exendin-4 (Ex-4) is a natural agonist of the glucagon-like peptide-1 (GLP-1) receptor, currently being used as a treatment for type 2 diabetes mellitus due to its insulinotropic properties. Previous studies have revealed that acute administration of both GLP-1 and, in particular, Ex-4 potently stimulates hypothalamic-pituitary-adrenal (HPA) axis activity. In this work, the effects of prolonged Ex-4 exposure on HPA function were explored. To this end, Sprague-Dawley rats were subjected to a daily regimen of two Ex-4 injections (5 μg/kg sc) for a minimum of 7 days. We found that subchronic Ex-4 administration produced a number of effects that resemble chronic stress situations, including hyperactivation of the HPA axis during the trough hours, disruption of glucocorticoid circadian secretion, hypertrophy of the adrenal gland, decreased adrenal gland sensitivity, impaired pituitary-adrenal stress responses, and reductions in both food intake and body weight. In addition, a threefold increase in diuresis was observed followed by a 1.5-fold increase in water intake; these latter effects were abolished by adrenalectomy. Together, these findings indicate that Ex-4 induces a profound dysregulation of HPA axis activity that may also affect renal function.

scholarly journals The Interaction between Maternal and Fetal Hypothalamic – Pituitary – Adrenal Axes

2021 ◽  
Author(s):  
Aml M. Erhuma
Keyword(s):  
Hpa Axis ◽  
Later Life ◽  
Postnatal Period ◽  
The Body ◽  
Prenatal Period ◽  
Hormonal Responses ◽  
Hypothalamic Pituitary Adrenal ◽  
External Threats ◽  
Unique System ◽  
Wide Range

The Hypothalamic – Pituitary – Adrenal (HPA) Axis is a unique system that mediates an immediate reactivity to a wide range of stimuli. It has a crucial role in synchronizing the behavioral and hormonal responses to internal and external threats, therefore, increases the chance of survival. It also enables the body systems to adapt to challenges put up by the pregnancy. Since the early stages of pregnancy and throughout delivery, HPA axis of the mother continuously navigates that of the fetus, and both have a specific cross talk even beyond the point of delivery and during postnatal period. Any disturbance in the interaction between the maternal and fetal HPA axes can adversely affect both. The HPA axis is argued to be the mechanism through which maternal stress and other suboptimal conditions during prenatal period can program the fetus for chronic disease in later life. In this chapter, the physiological and non-physiological communications between maternal and fetal HPA axes will be addressed while highlighting specific and unique aspects of this pathway.

Regulation of the hypothalamic-pituitary-adrenal axis by neuropeptides

2011 ◽  
Vol 7 (2) ◽  
Author(s):  
Greti Aguilera
Keyword(s):  
Hpa Axis ◽  
Fine Tuning ◽  
Metabolic Adaptation ◽  
Pituitary Hormone ◽  
Hypothalamic Pituitary Adrenal ◽  
External Zone ◽  
Adrenal Steroidogenesis ◽  
Pituitary Adenylate Cyclase ◽  
Response To Stress ◽  
Hpa Axis Activity

AbstractThe major endocrine response to stress occurs via activation of the hypothalamic-pituitary-adrenal (HPA) axis, leading ultimately to increases in circulating glucocorticoids, which are essential for the metabolic adaptation to stress. The major players in the HPA axis are the hypothalamic neuropeptide, corticotropin releasing hormone (CRH), the pituitary hormone adrenocorticotropic hormone, and the negative feedback effects of adrenal glucocorticoids. In addition, a number of other neuropeptides, including vasopressin (VP), angiotensin II, oxytocin, pituitary adenylate cyclase activating peptide, orexin and cholecystokinin, and nesfatin can affect HPA axis activity by influencing the expression and secretion of CRH, and also by modulating pituitary corticotroph function or adrenal steroidogenesis. Of these peptides, VP co-secreted with CRH from axonal terminals in the external zone of the median eminence plays a prominent role by potentiating the stimulatory effect of CRH and by increasing the number of pituitary corticotrophs during chronic challenge. Although the precise role and significance of many of these neuropeptides in regulating HPA axis activity requires further investigation, it is likely that they are part of a multifactorial system mediating the fine tuning of HPA axis activity during adaptation to a variety of physiological and stressful conditions.

scholarly journals Is there a gender difference in the associations of birthweight and adult hypothalamic–pituitary–adrenal axis activity?

2005 ◽  
Vol 152 (2) ◽  
pp. 249-253 ◽  
Author(s):  
Rebecca M Reynolds ◽  
Brian R Walker ◽  
Holly E Syddall ◽  
Ruth Andrew ◽  
Peter J Wood ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Plasma Cortisol ◽  
Low Birthweight ◽  
Low Dose ◽  
Birth Cohort Study ◽  
Men And Women ◽  
Hypothalamic Pituitary Adrenal ◽  
Adult Disease ◽  
Lower Birthweight ◽  
Hpa Axis Activity

Objective: Increased hypothalamic–pituitary–adrenal (HPA) axis activity in men of low birthweight may be an important link between early life and the adult metabolic syndrome. In animal models females are more sensitive than males to HPA axis programming, but whether gender influences susceptibility in humans is unknown. Design: Birth cohort study. Methods: We studied 106 women aged 67–78 years, from Hertfordshire, UK, in whom birthweight was recorded. Negative feedback sensitivity was assessed by an overnight low-dose (0.25 mg) dexa-methasone suppression test, and adrenal sensitivity by a low-dose (1 μg) ACTH1 – 24 stimulation test. Cortisol and its metabolites were analysed in a 24 h urine collection. Data were compared with previously published identical measurements in 205 men aged 66–77 years from the same cohort. Results: In women, plasma cortisol levels after dexamethasone were lower (P < 0.0001) and peak cortisol following ACTH1 – 24 were higher (P < 0.0001) than in men, suggesting a more responsive HPA axis. As in men, women with lower birthweight had enhanced plasma cortisol responses to ACTH1 – 24 (P = 0.05 for trend) but no difference in plasma cortisol after dexamethasone or in urinary cortisol metabolite excretion. The strength of the association in women was not different from that in men; a 1 lb decrease in birthweight was associated with an incremental rise in cortisol of 12.6 nmol/l (95% confidence interval (CI) 1.4, 23.8) in men, P = 0.03, and 14.8 nmol/l (95% CI −0.4, 29.9) in women, P = 0.05 (P = 0.82 for birthweight × gender interaction). In a combined analysis of men and women adjusted for gender (n = 302), a 1 lb decrease in birthweight was associated with a 13.4 nmol/l (95% CI 4.5, 22.4) greater incremental rise in plasma cortisol, P = 0.003. Conclusions: Associations between lower birthweight and increased HPA axis activity are similar in men and women, supporting the hypothesis that HPA axis activation is an important mechanism underlying programming of adult disease.

scholarly journals Featured Article: Community Crime Exposure and Risk for Obesity in Preschool Children: Moderation by the Hypothalamic–Pituitary–Adrenal-Axis Response

2017 ◽  
Vol 43 (4) ◽  
pp. 353-365 ◽  
Author(s):  
Maria A Gartstein ◽  
Erich Seamon ◽  
Stephanie F Thompson ◽  
Liliana J Lengua
Keyword(s):  
Risk Factors ◽  
Hpa Axis ◽  
Cumulative Risk ◽  
Unique Contribution ◽  
Neighborhood Crime ◽  
Diurnal Cortisol ◽  
Hypothalamic Pituitary Adrenal ◽  
Preschool Period ◽  
Child Bmi ◽  
Hpa Axis Activity

Abstract Objective Identification of early risk factors related to obesity is critical to preventative public health efforts. In this study, we investigated links between the Hypothalamic–Pituitary–Adrenal (HPA)-axis activity (diurnal cortisol pattern), geospatially operationalized exposure to neighborhood crime, and body mass index (BMI) for a sample of 5-year-old children. Greater community crime exposure and lower HPA-axis activity were hypothesized to contribute to higher BMI, with child HPA-axis moderating the association between crime exposure and BMI. Method Families residing within the boundaries of the City of Seattle (N = 114) provided information concerning demographic/psychosocial risk factors, used to calculate a Cumulative Risk Index, indicating the number of contextual adversities present. Child BMI and diurnal cortisol pattern (derived from assays of saliva samples) were examined, along with neighborhood crime indices computed with publically available information, based on participants’ locations. Results Hierarchical multiple regression analyses, adjusted for covariates (cumulative risk, age, and sex), indicated that crime proximity made a unique contribution to child BMI, in the direction signaling an increase in the risk for obesity. Consistent with our hypothesis, a significant interaction was observed, indicative of moderation by diurnal cortisol pattern. Follow-up simple slope analyses demonstrated that crime exposure was significantly related to higher BMI for children with low-flat (blunted) diurnal cortisol patterns, where community crime and BMI were not significantly associated at higher levels of cortisol. Conclusion Community crime exposure contributes to higher BMI as early as the preschool period, and blunted diurnal cortisol patterns may place children experiencing neighborhood adversity at greater risk for obesity.

Prenatal exposure to dexamethasone alters hippocampal drive on hypothalamic-pituitary-adrenal axis activity in adult male rats

2006 ◽  
Vol 290 (5) ◽  
pp. R1366-R1373 ◽  
Author(s):  
Jennifer A. Shoener ◽  
Romana Baig ◽  
Kathleen C. Page
Keyword(s):  
Hpa Axis ◽  
Adult Male ◽  
Restraint Stress ◽  
Exposed Group ◽  
Late Gestation ◽  
Male Rats ◽  
Mrna Levels ◽  
Hypothalamic Pituitary Adrenal ◽  
Hpa Axis Activity ◽  
Circulating Levels

Glucocorticoids are essential for normal hypothalamic-pituitary-adrenal (HPA) axis activity; however, recent studies warn that exposure to excess endogenous or synthetic glucocorticoid during a specific period of prenatal development adversely affects HPA axis stability. We administered dexamethasone (DEX) to pregnant rats during the last week of gestation and investigated subsequent HPA axis regulation in adult male offspring in unrestrained and restraint-stressed conditions. With the use of real-time PCR and RIA, we examined the expression of regulatory genes in the hippocampus, hypothalamus, and pituitary, including corticotropin-releasing hormone (CRH), arginine vasopressin (AVP), glucocorticoid receptors (GR), mineralcorticoid receptors (MR), and 11-β-hydroxysteroid dehydrogenase-1 (11β-HSD-1), as well as the main HPA axis hormones, adrenal corticotropic hormone (ACTH) and corticosterone (CORT). Our results demonstrate that the DEX-exposed group exhibited an overall change in the pattern of gene expression and hormone levels in the unrestrained animals. These changes included an upregulation of CRH in the hypothalamus, a downregulation of MR with a concomitant upregulation of 11β-HSD-1 in the hippocampus, and an increase in circulating levels of both ACTH and CORT relative to unrestrained control animals. Interestingly, both DEX-exposed and control rats exhibited an increase in pituitary GR mRNA levels following a 1-h recovery from restraint stress; however, the increased expression in DEX-exposed rats was significantly less and was associated with a slower return to baseline CORT compared with controls. In addition, circulating levels of ACTH and CORT as well as hypothalamic CRH and hippocampal 11β-HSD-1 expression levels were significantly higher in the DEX-exposed group compared with controls following restraint stress. Taken together, these data demonstrate that late-gestation DEX exposure in rats is associated with persistent changes in both the modulation of HPA axis activity and the HPA axis-mediated response to stress.

Multiple reciprocal relationships between in vivo cellular immunity and hypothalamic–pituitary–adrenal axis in depression

1994 ◽  
Vol 24 (1) ◽  
pp. 167-177 ◽  
Author(s):  
M. Maes ◽  
H. Y. Meltzer ◽  
W. Stevens ◽  
P. Cosyns ◽  
P. Blockx
Keyword(s):  
T Cells ◽  
Major Depression ◽  
Hpa Axis ◽  
Reciprocal Relationships ◽  
Hypothalamic Pituitary Adrenal ◽  
Hla Dr ◽  
Hpa Axis Activity ◽  
Increased Activity ◽  
Pituitary Adrenal Axis

SynopsisMajor depression is reportedly characterized by increased activity of the hypothalamic–pituitary–adrenal (HPA) axis and by in vivo immune activation. The present study was carried out in order to investigate the relationships between HPA-axis activity and in vivo immune function in depression. Towards this end the following parameters were measured: 24 h urinary cortisol (UC) excretion; basal and post-dexamethasone (DST) plasma cortisol, β-endorphin/β-lipotropin (βEND/βLPH) and dexamethasone concentrations; and leucocyte subsets (i.e. lymphocytes, neutrophils, monocytes, CD4+, CD4+CD45RA+, CD4+CD45RO+, CD8+, CD8+CD57+, CD8+CD57−, HLA-DR+, CD25+ T cells, HLA-DR+, CD19+, CD20+, and CD21+ B cells) both pre-and post-DST. Dexamethasone administration (1 mg orally) induced leucocytosis, lymphocytopaenia, monocytopaenia and neutrophilia. HPA-axis non-suppressors exhibited a relative resistance to the enhancing (e.g. neutrophils) or depressant (e.g. lymphocytes, CD4+ T cells) effects of dexamethasone. There were significant correlations between UC excretion and the number of percentage of lymphocytes, monocytes, CD4+CD45RA+ and CD8+CD57− T cells (negatively) and neutrophils (positively). It is concluded that multiple and complex intertwined relationships between HPA-axis hyperactivity and systemic immune stimulation participate in the pathophysiology or pathogenesis of major depression.

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