Hypothalamic–pituitary–adrenal (HPA) axis response to exogenous corticotropin‐releasing hormone (CRH) is attenuated in men with chronic insomnia

Eleven patients with major depression and 12 control subjects were administered corticotropin-releasing hormone (CRH), aqueous arginine vasopressin (AVP), and insulin hypoglycaemia (IH) to test for differences in hypothalamic–pituitary–adrenal (HPA) axis function. Patients with major depression demonstrated lower ACTH responses to CRH when compared with controls, and a trend toward such after administration of AVP. Despite lower ACTH responses in patients with depression, there were no differences in Cortisol responses to these stimuli. In the CRH and AVP tests, there was no correlation between the basal Cortisol and ACTH responses in either controls or patients, but in the IH test there was a negative correlation between these responses for both groups. The ACTH responses to CRH and AVP were positively correlated in controls and patients. Cortisol responses to all three provocative stimuli were positively correlated in both subject groups. These findings are consistent with the hypothesis that hypothalamic or supra-hypothalamic overactivity may be involved in the development of HPA-axis abnormalities in patients with depression.

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THE HYPOTHALAMIC-PITUITARY-ADRENAL (HPA) AXIS OF PATIENTS WITH SEVERE SEPSIS: ALTERED RESPONSE TO CORTICOTROPIN-RELEASING HORMONE (CRH)

Critical Care Medicine ◽

10.1097/00003246-199912001-00408 ◽

1999 ◽

Vol 27 (Supplement) ◽

pp. A144

Author(s):

Stefan Schroeder ◽

Maria Wichers ◽

Lutz E Lehmann ◽

Christian Putensen ◽

Andreas Hoeft ◽

...

Keyword(s):

Severe Sepsis ◽

Hpa Axis ◽

Corticotropin Releasing Hormone ◽

Hypothalamic Pituitary Adrenal ◽

Releasing Hormone ◽

Altered Response

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The Nutrient and Energy Sensor Sirt1 Regulates the Hypothalamic-Pituitary-Adrenal (HPA) Axis by Altering the Production of the Prohormone Convertase 2 (PC2) Essential in the Maturation of Corticotropin-releasing Hormone (CRH) from Its Prohormone in Male Rats

Journal of Biological Chemistry ◽

10.1074/jbc.m115.675264 ◽

2016 ◽

Vol 291 (11) ◽

pp. 5844-5859 ◽

Cited By ~ 11

Author(s):

Anika M. Toorie ◽

Nicole E. Cyr ◽

Jennifer S. Steger ◽

Ross Beckman ◽

George Farah ◽

...

Keyword(s):

Hpa Axis ◽

Male Rats ◽

Prohormone Convertase ◽

Corticotropin Releasing Hormone ◽

Hypothalamic Pituitary Adrenal ◽

Releasing Hormone ◽

Energy Sensor ◽

Prohormone Convertase 2

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New effects of caffeine on corticotropin‐releasing hormone (CRH)‐induced stress along the intrafollicular classical hypothalamic–pituitary–adrenal (HPA) axis (CRH‐R1/2, IP 3 ‐R, ACTH, MC‐R2) and the neurogenic non‐HPA axis (substance P, p75 NTR and TrkA) in ex vivo human male androgenetic scalp hair follicles

British Journal of Dermatology ◽

10.1111/bjd.19115 ◽

2020 ◽

Cited By ~ 1

Author(s):

T.W. Fischer ◽

A. Bergmann ◽

N. Kruse ◽

K. Kleszczynski ◽

C. Skobowiat ◽

...

Keyword(s):

Substance P ◽

Hpa Axis ◽

Scalp Hair ◽

Ex Vivo ◽

Hair Follicles ◽

Corticotropin Releasing Hormone ◽

Hypothalamic Pituitary Adrenal ◽

Releasing Hormone ◽

Human Male ◽

Induced Stress

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Gonadotropin-releasing hormone agonist in premenopausal women does not alter hypothalamic-pituitary-adrenal axis response to corticotropin-releasing hormone

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00221.2017 ◽

2018 ◽

Vol 315 (2) ◽

pp. E316-E325 ◽

Cited By ~ 2

Author(s):

Kathleen M. Gavin ◽

Karen L. Shea ◽

Ellie Gibbons ◽

Pamela Wolfe ◽

Robert S. Schwartz ◽

...

Keyword(s):

Hpa Axis ◽

Area Under The Curve ◽

Premenopausal Women ◽

Gonadotropin Releasing Hormone ◽

Corticotropin Releasing Hormone ◽

Hypothalamic Pituitary Adrenal ◽

Releasing Hormone ◽

Gonadotropin Releasing Hormone Agonist ◽

Total Cortisol ◽

Hpa Axis Activity

Sex hormones appear to play a role in the regulation of hypothalamic-pituitary-adrenal (HPA) axis activity. The objective was to isolate the effects of estradiol (E2) on central activation of the HPA axis. We hypothesized that the HPA axis response to corticotropin-releasing hormone (CRH) under dexamethasone (Dex) suppression would be exaggerated in response to chronic ovarian hormone suppression and that physiologic E2 add-back would mitigate this response. Thirty premenopausal women underwent 20 wk of gonadotropin-releasing hormone agonist therapy (GnRHAG) and transdermal E2 (0.075 mg per day, GnRHAG + E2, n = 15) or placebo (PL) patch (GnRHAG + PL, n = 15). Women in the GnRHAG + PL and GnRHAG + E2 groups were of similar age (38 (SD 5) yr vs. 36 (SD 7) yr) and body mass index (27 (SD 6) kg/m2 vs. 27 (SD 6) kg/m2). Serum E2 changed differently between the groups ( P = 0.01); it decreased in response to GnRHAG + PL (77.9 ± 17.4 to 23.2 ± 2.6 pg/ml; P = 0.008) and did not change in response to GnRHAG + E2 (70.6 ± 12.4 to 105 ± 30.4 pg/ml; P = 0.36). The incremental area under the curve (AUCINC) responses to CRH were different between the groups for total cortisol ( P = 0.03) and cortisone ( P = 0.04) but not serum adrenocorticotropic hormone (ACTH) ( P = 0.28). When examining within-group changes, GnRHAG + PL did not alter the HPA axis response to Dex/CRH, but GnRHAG + E2 decreased the AUCINC for ACTH (AUCINC, 1,623 ± 257 to 1,211 ± 236 pg/ml·min, P = 0.004), cortisone (1,795 ± 367 to 1,090 ± 281 ng/ml·min, P = 0.009), and total cortisol (7,008 ± 1,387 to 3,893 ± 1,090 ng/ml·min, P = 0.02). Suppression of ovarian hormones by GnRHAG therapy for 20 wk did not exaggerate the HPA axis response to CRH, but physiologic E2 add-back reduced HPA axis activity compared with preintervention levels.

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