Cited by 275Platelet Disorders and TreatmentsCardiovascular, Neuropeptides, and Oxidative Stress ResearchBlood Coagulation and Thrombosis Mechanisms

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Vasopressin-induced von Willebrand factor secretion from endothelial cells involves V2 receptors and cAMP

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Kaufmann, Jocelyne E., Oksche, Alexander, Wollheim, Claes B., Günther, Gabriele, Rosenthal, Walter, Vischer, Ulrich M.·2000·Journal of Clinical Investigation

DOI 10.1172/jci9516PMC PMC314363

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Abstract

Vasopressin and its analogue 1-deamino-8-D-arginine vasopressin (DDAVP) are known to raise plasma von Willebrand factor (vWF) levels. DDAVP is used as a hemostatic agent for the treatment of von Willebrand's disease. However, its cellular mechanisms of action have not been elucidated. DDAVP, a specific agonist for the vasopressin V2 receptor (V2R), exerts its antidiuretic effect via a rise in cAMP in kidney collecting ducts. We tested the hypothesis that DDAVP induces vWF secretion by binding to V2R and activating cAMP-mediated signaling in endothelial cells. vWF secretion from human umbilical vein endothelial cells (HUVECs) can be mediated by cAMP, but DDAVP is ineffective, presumably due to the absence of V2R. We report that DDAVP stimulates vWF secretion in a cAMP-dependent manner in HUVECs after transfection of the V2R. In addition, vasopressin and DDAVP induce vWF secretion in human lung microvascular endothelial cells (HMVEC-L). These cells (but not HUVECs) express endogenous V2R, as shown by RT-PCR. Vasopressin-induced vWF secretion is mimicked by DDAVP and inhibited by the selective V2R antagonist SR121463B. It is mediated by cAMP, since it is inhibited by the protein kinase A inhibitor Rp-8CPT-cAMPS. These results indicate that vasopressin induces cAMP-mediated vWF secretion by a direct effect on endothelial cells. They also demonstrate functional expression of V2R in endothelial cells, and provide a cellular mechanism for the hemostatic effects of DDAVP.

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Authors: Kaufmann, J. E., Oksche, A., Wollheim, C. B., Günther, G., Rosenthal, W., & Vischer, U. M.
Affiliations: University of Geneva (CH)
Leibniz-Forschungsinstitut für Molekulare Pharmakologie (DE)
Corresponding author: Kaufmann, Jocelyne E.
ORCID: Oksche, Alexander
Wollheim, Claes B.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2000-07-01
Volume: 106
Issue: 1
Pages: 107-116
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci9516
PMC: PMC314363
OpenAlex: W2052753575
Cited by: 275
References: 47
Citations by year: 2026: 5 · 2025: 9 · 2024: 6 · 2023: 14 · 2022: 11 · 2021: 12 · 2020: 12 · 2019: 9 · 2018: 15 · 2017: 7 · 2016: 13 · 2015: 12 · 2014: 13 · 2013: 15 · 2012: 8
FWCI: 4.71
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Archive ouverte UNIGE (University of Geneva) (publishedVersion, other-oa)
Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
Funders: Fonds National de la Recherche Luxembourg
Helmut Horten Stiftung
Topics: Health Sciences › Medicine › Hematology › Platelet Disorders and Treatments
Health Sciences › Medicine › Surgery › Cardiovascular, Neuropeptides, and Oxidative Stress Research
Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
Keywords: vasopressin, von Willebrand factor secretion, V2 receptor, cAMP signaling, protein kinase A, endothelial cells, desmopressin, von Willebrand disease, hemostasis, lung microvascular endothelial cells
MeSH terms: Cyclic AMP, Arginine Vasopressin, Cells, Cultured, Deamino Arginine Vasopressin, Endothelium, Vascular, Humans, Lung, RNA, Messenger, von Willebrand Factor, Receptors, Vasopressin, Reverse Transcriptase Polymerase Chain Reaction

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Vasopressin-induced von Willebrand factor secretion from endothelial cells involves V2 receptors and cAMP

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