Cited by 26Stress Responses and CortisolAdrenal Hormones and DisordersNeuroendocrine regulation and behavior

Magnocellular vasopressin and the mechanism of “Glucocorticoid escape”

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Antoni, Ferenc A.·2019·Frontiers in Endocrinology

Abstract

It is now widely accepted that magnocellular vasopressinergic neurons in the supraoptic and paraventricular nuclei participate in the control of adrenocorticotropin secretion by the anterior pituitary gland. However, it remains to be explored in further detail, when and how these multifunctional neurons are involved in the control of anterior pituitary function. This paper highlights the role of magnocellular vasopressin in the hypothalamic pituitary adrenocortical axis with special reference to escape from glucocorticoid feedback inhibition. The signaling mechanisms underlying glucocorticoid escape by pituitary corticotrope cells, as well as the wider physiologic and pathologic contexts in which escape is known to occur-namely strenuous exercise, and autoimmune inflammation will be considered. It is proposed that by inducing escape from glucocorticoid feedback inhibition at the pituitary level, magnocellular vasopressin is critically important for the anti-inflammatory, and immunosuppressant actions of endogenous corticosteroids.

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Crossref · 10.3389/fendo.2019.00422

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  • 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 [51]

    The ‘Signal Integration by Corticotrope Cells’ section (page unavailable) says that stimulatory input comprises CRF and VP, and the stress-response section reports an important role for VP in stress-induced ACTH secretion. The paper does not establish that both inputs are required for a complete ACTH response under normal conditions and across various stressors; it also describes CRF-induced ACTH release without VP. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • Magnocellular neurons are not under prominent negative feedback control by adrenal corticosteroids.

    “Furthermore, these neurons are not under prominent negative feedback control by adrenal corticosteroids (51).”
  • Inflow of AVP from magnocellular neurons can be much more abundant (up to 10-fold) than from parvocellular neurons under normal conditions.

    “On the other hand, inflow of AVP from the magnocellular neurons (R4) can be much more abundant (up to 10-fold) than from parvocellular neurons under normal condition (51).”

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References 90 · Cited by 26

Authors
Antoni, F. A.
Affiliations
University of Edinburgh (GB)
Corresponding author
Antoni, Ferenc A.
Venue
Frontiers in Endocrinology
Published
2019-06-26
Volume
10
Pages
422-422
ISSN
1664-2392 (ISSN-L)
OpenAlex
W2954234941
Cited by
26
References
90
Citations by year
2026: 1 · 2025: 4 · 2024: 5 · 2023: 3 · 2022: 9 · 2021: 2 · 2020: 2
FWCI
0.38
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Endocrinology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
Funders
Semmelweis Egyetem
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
  • Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
Keywords
adrenocorticotropin secretion, anterior pituitary, hypothalamic-pituitary-adrenal axis, supraoptic nucleus, paraventricular nucleus, glucocorticoid feedback inhibition, physical activity, autoimmune inflammation, immunosuppression

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