Cited by 138Stress Responses and CortisolNeuropeptides and Animal PhysiologyNeuroendocrine regulation and behavior

Vasopressinergic regulation of the hypothalamic pituitary adrenal axis and stress adaptation

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Volpi, Simona, Rabadan-Diehl, Cristina, Aguilera, Greti·2004·Stress

Abstract

Vasopressin (VP) stimulates pituitary ACTH secretion through interaction with receptors of the V1b subtype (V1bR, V3R), located in the plasma membrane of the pituitary corticotroph, mainly by potentiating the stimulatory effects of corticotropin releasing hormone (CRH). Chronic stress paradigms associated with corticotroph hyperresponsiveness lead to preferential expression of hypothalamic VP over CRH and upregulation of pituitary V1bR, suggesting an important role for VP during adaptation of the hypothalamic-pituitary-adrenal (HPA) axis to stress. Vasopressinergic regulation of ACTH secretion depends on the number of V1bRs as well as coupling of the receptor to phospholipase C (PLC) in the pituitary. Regulation of V1bR gene transcription may involve a number of regulatory elements in the promoter region, of which a GAGA box was shown to be essential. Although V1bR gene transcription is necessary to maintain V1bR mRNA levels, the lack of correlation between VP binding and V1bR mRNA suggests that regulation of mRNA translation is a major regulatory step of the number of V1bRs. V1bR translation appears to be under tonic inhibition by upstream minicistrons and positive regulation through protein kinase C (PKC) activation of an internal ribosome entry site (IRES) in the 5' untranslated region (5'UTR) of the mRNA. The data provide mechanisms by which regulation of hypothalamic VP and pituitary V1bR content contribute to controlling HPA axis activity during chronic stress.

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Crossref · 10.1080/10253890410001733535

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  • Both CRH and AVP act on their own receptors on corticotrope cells in the anterior pituitary to stimulate ACTH production and release, with different or even similar potencies.

    “Namely, it has been indicated that both CRH and AVP act on their own receptors (28–32) on corticotrope cells in anterior pituitary to stimulate adrenocorticotropic hormone (ACTH) production and release with different (26, 33–41) or even similar potencies (42).”

    From Influence of arginine vasopressin on the ultradian dynamics of Hypothalamic-Pituitary-Adrenal axis (2022) · cites this paper as [32]

    The ‘Vasopressinergic Regulation of the Pituitary Corticotroph’ section (page unavailable) supports ACTH secretion by both hormones but says VP alone is a weak stimulus that potentiates CRH, not that they have similar potencies. It also says VP inhibits basal and CRH-stimulated POMC gene transcription, so the claim that both stimulate ACTH production is not supported. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • CRH and AVP are both required as stimulatory inputs to corticotrope cells for a complete ACTH response in physiologically normal and various stressful conditions.

    “In essence, CRH and AVP are both required as stimulatory inputs to corticotrope cells for a complete ACTH response in physiologically normal as well as in various stressful conditions (32, 38, 48–51).”

    From Influence of arginine vasopressin on the ultradian dynamics of Hypothalamic-Pituitary-Adrenal axis (2022) · cites this paper as [32]

    The Introduction and “Vasopressinergic Regulation of the Pituitary Corticotroph” section (pages unavailable) say that vasopressin potentiates CRH-stimulated ACTH secretion and helps maintain corticotroph responsiveness during chronic stress. They do not establish that both inputs are required for a complete ACTH response under physiologically normal conditions or across various stressful conditions. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

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1 of the 60 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. Sonnenberg, N. (1996) In: Hershey, J.W.B., Mathews, M.B. and Sonenberg, N., eds, Translational Control (Cold Spring Harbor Lab. Press, Plainview, NY), pp 245-269.

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Authors
Volpi, S., Rabadan-Diehl, C., & Aguilera, G.
Affiliations
National Institutes of Health (US)
Corresponding author
Aguilera, Greti
Venue
Stress
Published
2004-06
Volume
7
Issue
2
Pages
75-83
ISSN
  • 1025-3890 (ISSN-L)
  • 1607-8888
OpenAlex
W2094450224
Cited by
136
References
60
Citations by year
2026: 1 · 2025: 4 · 2024: 2 · 2023: 4 · 2022: 10 · 2021: 5 · 2020: 3 · 2019: 4 · 2018: 7 · 2017: 6 · 2016: 4 · 2015: 5 · 2014: 6 · 2013: 9 · 2012: 3
FWCI
0.70
Type
journal article
Language
en
Open access
Licence
public-domain
Locations
  • Stress (publishedVersion, public-domain)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
  • Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
Keywords
vasopressin, V1b receptor, hypothalamic-pituitary-adrenal axis, ACTH secretion, corticotropin-releasing factor, chronic stress, stress adaptation, phospholipase C signaling, mRNA translation regulation, protein kinase C, internal ribosome entry site, 5' untranslated region
MeSH terms
Adaptation, Physiological, Animals, Humans, Hypothalamo-Hypophyseal System, Pituitary-Adrenal System, Stress, Physiological, Vasopressins

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