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Vasopressinergic Regulation of the Hypothalamic Pituitary Adrenal Axis and Stress Adaptation
Open accessAbstract
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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“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]
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“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]
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Citations
Cites
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Background
Metadata
- Authors
- Volpi, S., Rabadan-Diehl, C., & Aguilera, G.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Aguilera, Greti
- ORCID
- Volpi, Simona
- Venue
- Stress
- Publisher
- Informa UK Limited
- 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
- hybrid
- doi.org
- 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
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › 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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