Cited by 25Neuroendocrine regulation and behaviorNeuropeptides and Animal PhysiologyStress Responses and Cortisol

Effects of vasopressin V1b receptor deficiency on adrenocorticotropin release from anterior pituitary cells in response to oxytocin stimulation

Nakamura, Kazuaki, Fujiwara, Yoko, Mizutani, Reiko, Sanbe, Atsushi, Miyauchi, Noriko, Hiroyama, Masami, Yamauchi, Junji, Yamashita, Tatsuya +4 more·2008·Endocrinology

Abstract

Oxytocin (OT) is one of the secretagogues for stress-induced ACTH release. OT-induced ACTH release is reported to be mediated by the vasopressin V1b receptor in the rat pituitary gland, which contains both OT and V1b receptors. We examined OT-induced ACTH release using primary cultures of anterior pituitary cells from wild-type (V1bR+/+) and V1b receptor knockout (V1bR-/-) mice. OT stimulated similar levels of ACTH release from pituitary cells of V1bR+/+ and V1bR-/- mice. OT-induced ACTH release was significantly inhibited by the selective V1b receptor antagonist SSR149415 and the OT receptor antagonist CL-14-26 in V1bR+/+ mice. In addition, cotreatment with SSR149415 at 10(-6) m and CL-14-26 at 10(-6) m inhibited OT-induced ACTH release to the control level inV1bR+/+ mice. In V1bR-/- mice, OT-induced ACTH release was significantly inhibited by CL-14-26 at 10(-8) m and completely inhibited at 10(-7)m. These results indicate that OT induces the ACTH response via OT and V1b receptors inV1bR+/+ mice but via only OT receptors in V1bR-/- mice. The gene expression level of the OT receptor was significantly higher in the anterior pituitary gland of V1bR-/- mice than in that of V1bR+/+ mice, suggesting that the OT receptor is up-regulated to compensate for ACTH release under conditions of V1b receptor deficiency.

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Crossref · 10.1210/en.2007-1528

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Authors
Nakamura, K., Fujiwara, Y., Mizutani, R., Sanbe, A., Miyauchi, N., Hiroyama, M., Yamauchi, J., Yamashita, T., Nakamura, S., Mori, T., Tsujimoto, G., & Tanoue, A.
Affiliations
  • National Research Institute for Child Health and Development (JP)
  • Otsuka Pharmaceutical Co., Ltd. (T.Y., S.N., T.M.), Kawauchi-cho Tokushima 771-0192, Japan
  • Kyoto University (JP)
Corresponding author
Tanoue, Akito
Venue
Endocrinology
Published
2008-06-26
Volume
149
Issue
10
Pages
4883-4891
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
OpenAlex
W2020140739
Cited by
25
References
37
Citations by year
2021: 1 · 2019: 1 · 2018: 3 · 2017: 4 · 2014: 2 · 2013: 2 · 2012: 4
FWCI
3.57
Type
journal article
Language
en
Open access
closed
Locations
  • Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
vasopressin V1b receptor, oxytocin, anterior pituitary cells, oxytocin receptor, receptor knockout mice
MeSH terms
Adrenocorticotropic Hormone, Animals, Cells, Cultured, Indoles, Male, Oxytocin, Pituitary Gland, Anterior, Pyrrolidines, RNA, Messenger, Up-Regulation, Gene Expression, Receptors, Vasopressin, Receptors, Oxytocin, Mice, Knockout, Reverse Transcriptase Polymerase Chain Reaction, Mice

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