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Cited by 105Pancreatic function and diabetesNeuropeptides and Animal PhysiologyNeuroendocrine regulation and behavior

Vasopressin stimulates insulin release from islet cells through V1b receptors: a combined pharmacological/knockout approach

Oshikawa, Sayuri, Tanoue, Akito, Koshimizu, Taka-aki, Kitagawa, Yoko, Tsujimoto, Gozoh·2004·Molecular Pharmacology
DOI 10.1124/mol.65.3.623
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Abstract

Vasopressin receptor subtype(s) responsible for stimulation of insulin release from pancreatic beta cells were investigated by using subtype-selective antagonists and mice that were genetically lacking either V1a or V1b receptors. Arginine vasopressin (AVP) increased insulin release from isolated mouse islet cells in a concentration-dependent manner, with a submaximal response at 100 nM. Reverse transcription-polymerase chain reaction (RT-PCR) analysis detected V1b and oxytocin, but not V1a or V2, receptor transcripts in mouse islet cells. We characterized the recently synthesized vasopressin receptor subtype antagonists (2S)1-[(2R 3S)-(5-chloro-3-(2-chlorophenyl)-1-(3,4-dimethoxybenzene-sulfonyl)-3-hydroxy-2,3-difydro-1H-indole-2-carbonyl)-pyrrolidine-2-carboxamide] (SR49059), 1-[1-[4-(3-acetylaminopropoxy)benzoyl]-4-piperidyl]-3,4-dihydro-2(1H)-quinolinone (OPC-21268), and (2S,4R)-1-[5-chloro-1-[(2,4-dimethoxyphenyl)sulfonyl]-3-(2-methoxy-phenyl)-2-oxo-2,3-dihydro-1H-indol-3-yl]-4-hydroxy-N,N-dimethyl-2-pyrrolidine carboxamide (SSR149415) using human embryonic kidney 293 cells stably expressing the three cloned mouse vasopressin receptors (V1a, V1b, and V2). A radioligand binding study showed that SR49059 and OPC-21268 potently inhibited [3H]AVP binding to the cloned mouse V1a receptor, with Ki values of 27 and 510 nM, respectively, whereas SSR149415 potently inhibited [3H]AVP binding to the cloned mouse V1b receptor with a Ki value of 110 nM. The inhibitory effects of vasopressin antagonists on AVP-induced insulin release correlate well with the rank order of potency to inhibit [3H]AVP binding to the V1b receptor; pancreatic islet cells were significantly inhibited by SSR149415 but not by SR49059 or OPC-21268. Furthermore, the AVP effect on insulin release was entirely lost in mice lacking the V1b receptor but was preserved in mice lacking the V1a receptor. Our study, which combined pharmacological and knockout approaches, clearly demonstrates that vasopressin-stimulated insulin release from islet cells is mediated via V1b receptors.

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  • Vasopressin induces gluconeogenesis in the rat liver.

    “A causal link between vasopressin and glucose homeostasis is plausible because vasopressin induces gluconeogenesis in the rat liver and transiently increases glycemia in healthy humans and because vasopressin receptors are expressed in hepatocytes and pancreatic islets (2–9).”

    From Low Water Intake and Risk for New-Onset Hyperglycemia (2011) · cites this paper as [9]

  • A causal link between vasopressin and glucose homeostasis is plausible.

    “A causal link between vasopressin and glucose homeostasis is plausible because vasopressin induces gluconeogenesis in the rat liver and transiently increases glycemia in healthy humans and because vasopressin receptors are expressed in hepatocytes and pancreatic islets (2–9).”

    From Low Water Intake and Risk for New-Onset Hyperglycemia (2011) · cites this paper as [9]

  • Vasopressin receptors are expressed in hepatocytes and pancreatic islets.

    “A causal link between vasopressin and glucose homeostasis is plausible because vasopressin induces gluconeogenesis in the rat liver and transiently increases glycemia in healthy humans and because vasopressin receptors are expressed in hepatocytes and pancreatic islets (2–9).”

    From Low Water Intake and Risk for New-Onset Hyperglycemia (2011) · cites this paper as [9]

  • Vasopressin transiently increases glycemia in healthy humans.

    “A causal link between vasopressin and glucose homeostasis is plausible because vasopressin induces gluconeogenesis in the rat liver and transiently increases glycemia in healthy humans and because vasopressin receptors are expressed in hepatocytes and pancreatic islets (2–9).”

    From Low Water Intake and Risk for New-Onset Hyperglycemia (2011) · cites this paper as [9]

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Authors
Oshikawa, S., Tanoue, A., Koshimizu, T.-A., Kitagawa, Y., & Tsujimoto, G.
Affiliations
National Research Institute for Child Health and Development (JP)
ORCID
Venue
Molecular Pharmacology
Publisher
Elsevier BV
Published
2004-03
Volume
65
Issue
3
Pages
623-629
ISSN
0026-895X (ISSN-L)
DOI
10.1124/mol.65.3.623
OpenAlex
W2128253171
Cited by
105
References
44
Citations by year
2025: 6 · 2024: 3 · 2023: 6 · 2022: 1 · 2021: 5 · 2020: 3 · 2019: 4 · 2018: 3 · 2017: 5 · 2016: 8 · 2015: 7 · 2014: 1 · 2013: 10 · 2012: 3
FWCI
6.15
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Molecular Pharmacology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Otsuka Pharmaceutical
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
  • Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
Keywords
vasopressin, insulin secretion, pancreatic beta cells, V1b receptor, V1a receptor, vasopressin receptor antagonists, OPC-21268, receptor subtype selectivity, knockout mice, oxytocin, pancreatic endocrine cells
MeSH terms
Animals, Arginine Vasopressin, Binding Sites, Cells, Cultured, Humans, Insulin, Islets of Langerhans, RNA, Messenger, Vasopressins, Receptors, Vasopressin, Mice, Knockout, Mice, Antidiuretic Hormone Receptor Antagonists

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