Cited by 127Neuroendocrine regulation and behaviorNeuropeptides and Animal PhysiologyCardiovascular, Neuropeptides, and Oxidative Stress Research

The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.

Localization of Vasopressin Binding Sites in Rat Tissues Using Specific Vi and V2 Selective Ligands*

Abstract

Arginine vasopressin (AVP) acts on at least two receptor types, classified on the basis of their second messengers. The V1 receptor acts via mobilization of intracellular calcium through phosphatidylinositol hydrolysis and influences blood pressure and hepatic glycogenolysis. The V2 receptor acts via cAMP through activation of adenylate cyclase and causes antidiuresis. Previous studies of the different AVP receptors have been hampered by the use of nonselective radioligands, such as [3H]AVP (which binds to all types of V1 and V2 receptors, certain oxytocin receptors, and neurophysins) as well as the difficulty of measurement of second messengers. This paper describes the use of selective V1 and V2 radioligands with in vitro autoradiography to study V1 and V2 binding sites in rat tissues. [125I][1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 7-sarcosine] arginine vasopressin ([125I][d(CH2)5,Sarcosine7]AVP), a selective V1 antagonist radioligand, bound to regions of the brain, testis, superior cervical ganglion, liver, blood vessels, and renal medulla. Pharmacological characterization of [125I][d(CH2)5,Sarcosine7]AVP binding was consistent with that expected for binding to V1 receptors. There was no specific binding demonstrable to pituitary, renal glomeruli, gut, heart, spinal cord, ovary, adrenal medulla, or adrenal cortex. [3H]1-deamino [8-D-arginine] vasopressin [( 3H]DDAVP), a potent V2 receptor agonist radioligand, was used to study V2 receptors. Specific binding was only identified in the kidney consistent with the known distribution of antidiuretic V2 receptors on renal collecting tubules. No binding was demonstrated on endothelium or liver where DDAVP might influence clotting factor release, nor in the brain, spinal cord, sympathetic ganglia, heart or vascular smooth muscle, regions where DDAVP might cause vasodilatation. These studies demonstrate the use of these radioligands to study V1 and V2 receptors in a variety of tissues. Also, since these ligands are selective they are of particular use to study the different receptor subtypes in tissues where V1 and V2 receptors coexist, such as in the kidney.

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Crossref · 10.1210/endo-126-3-1478

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33 of 33 references verified0 citation errors · 0 not checkable

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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 [6]

  • 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 [6]

  • 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 [6]

  • 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 [6]

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Metadata

Authors
PHILLIPS, P. A., ABRAHAMS, J. M., KELLY, J. M., MOOSER, V., TRINDER, D., & JOHNSTON, C. I.
Affiliations
The University of Melbourne (AU)
Venue
Endocrinology
Published
1990-03
Volume
126
Issue
3
Pages
1478-1484
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
OpenAlex
W1997729156
Cited by
127
References
33
Citations by year
2026: 3 · 2025: 2 · 2024: 1 · 2023: 3 · 2022: 2 · 2021: 5 · 2020: 1 · 2019: 2 · 2017: 1 · 2016: 1 · 2015: 2 · 2014: 1 · 2013: 2 · 2012: 2
FWCI
16.40
Type
journal article
Language
en
Open access
closed
Locations
  • Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroendocrine regulation and behavior
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
  • Health Sciences › Medicine › Surgery › Cardiovascular, Neuropeptides, and Oxidative Stress Research
Keywords
V1 receptor, V2 receptor, receptor localization, desmopressin, vasopressin, in vitro autoradiography, rat tissues, receptor subtypes
MeSH terms
Animals, Autoradiography, Binding Sites, Blood Vessels, Brain, Kidney Glomerulus, Ligands, Liver, Membranes, Rats, Inbred Strains, Vasopressins, Rats

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