scholarly journals A snake toxin as a theranostic agent for the type 2 vasopressin receptor

Theranostics ◽  
2020 ◽  
Vol 10 (25) ◽  
pp. 11580-11594
Author(s):  
Laura Droctové ◽  
Manon Lancien ◽  
Vu Long Tran ◽  
Michaël Susset ◽  
Benoit Jego ◽  
...  
Keyword(s):  
Vasopressin Receptor ◽  
Theranostic Agent ◽  
Snake Toxin

scholarly journals Noncanonical Control of Vasopressin Receptor Type 2 Signaling by Retromer and Arrestin

2013 ◽  
Vol 288 (39) ◽  
pp. 27849-27860 ◽  
Author(s):  
Timothy N. Feinstein ◽  
Naofumi Yui ◽  
Matthew J. Webber ◽  
Vanessa L. Wehbi ◽  
Hilary P. Stevenson ◽  
...  
Keyword(s):  
Receptor Type ◽  
Vasopressin Receptor

scholarly journals Role of pendrin in iodide balance: going with the flow

2009 ◽  
Vol 297 (4) ◽  
pp. F1069-F1079 ◽  
Author(s):  
Young Hee Kim ◽  
Truyen D. Pham ◽  
Wencui Zheng ◽  
Seongun Hong ◽  
Christine Baylis ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Water Intake ◽  
Apical Plasma Membrane ◽  
Vasopressin Receptor ◽  
Intercalated Cells ◽  
Type B ◽  
Wild Type ◽  
Dependent Mechanism

Pendrin is expressed in the apical regions of type B and non-A, non-B intercalated cells, where it mediates Cl−absorption and HCO3−secretion through apical Cl−/HCO3−exchange. Since pendrin is a robust I−transporter, we asked whether pendrin is upregulated with dietary I−restriction and whether it modulates I−balance. Thus I−balance was determined in pendrin null and in wild-type mice. Pendrin abundance was evaluated with immunoblots, immunohistochemistry, and immunogold cytochemistry with morphometric analysis. While pendrin abundance was unchanged when dietary I−intake was varied over the physiological range, I−balance differed in pendrin null and in wild-type mice. Serum I−was lower, while I−excretion was higher in pendrin null relative to wild-type mice, consistent with a role of pendrin in renal I−absorption. Increased H2O intake enhanced differences between wild-type and pendrin null mice in I−balance, suggesting that H2O intake modulates pendrin abundance. Raising water intake from ∼4 to ∼11 ml/day increased the ratio of B cell apical plasma membrane to cytoplasm pendrin label by 75%, although circulating renin, aldosterone, and serum osmolality were unchanged. Further studies asked whether H2O intake modulates pendrin through the action of AVP. We observed that H2O intake modulated pendrin abundance even when circulating vasopressin levels were clamped. We conclude that H2O intake modulates pendrin abundance, although not likely through a direct, type 2 vasopressin receptor-dependent mechanism. As water intake rises, pendrin becomes increasingly critical in the maintenance of Cl−and I−balance.

scholarly journals Thirst perception and arginine vasopressin production in a kindred with an activating mutation of the type 2 vasopressin receptor: the pathophysiology of nephrogenic syndrome of inappropriate antidiuresis

2009 ◽  
Vol 161 (3) ◽  
pp. 503-508 ◽  
Author(s):  
S Gupta ◽  
T D Cheetham ◽  
H J Lambert ◽  
C Roberts ◽  
D Bourn ◽  
...  
Keyword(s):  
Arginine Vasopressin ◽  
Receptor Gene ◽  
Vasopressin Receptor ◽  
Water Load ◽  
Activating Mutations ◽  
Activating Mutation ◽  
Mother And Child ◽  
Inappropriate Antidiuresis ◽  
Female Carriers

BackgroundActivating mutations of the vasopressin receptor gene on the X chromosome cause the nephrogenic syndrome of inappropriate antidiuresis (NSIAD). We describe a male child who presented with persistent hyponatraemia and whose mother was also found to be hyponatraemic. She had learnt to avoid excess fluid consumption because of associated malaise. Both individuals had a subnormal ability to excrete a water load with mother also demonstrating a heightened sense of thirst at low serum osmolalities.ResultsMother and child were found to have the previously characterised activating mutation (p.Arg137Cys) of the arginine vasopressin receptor type 2 gene (AVPR2), but had measurable levels of AVP when hyponatraemic.ConclusionsWe conclude that female carriers of activating mutations of the vasopressin receptor are susceptible to hyponatraemia and therefore need to be provided with advice regarding fluid intake. An altered thirst perception may increase susceptibility to hyponatraemia. We confirm that the presence of measurable amounts of AVP in patients with hyponatraemia does not exclude the diagnosis of  NSIAD.

scholarly journals Cellular and Subcellular Localization of the Type 2 Vasopressin Receptor in Kidney

2006 ◽  
Vol 20 (5) ◽  
Author(s):  
Robert Andrew Fenton ◽  
Lone Brønd ◽  
Jeppe Praetorius ◽  
Søren Nielsen
Keyword(s):  
Subcellular Localization ◽  
Vasopressin Receptor

Cloning of the Human Type-2 Vasopressin Receptor Gene

1993 ◽  
Vol 689 (1 The Neurohypo) ◽  
pp. 570-572 ◽  
Author(s):  
ANITA SEIBOLD ◽  
WALTER ROSENTHAL ◽  
CLAUDE BARBERIS ◽  
MARIEL BIRIEL BIRNBAUMER
Keyword(s):  
Receptor Gene ◽  
Vasopressin Receptor ◽  
Human Type

scholarly journals Green mamba peptide targets type-2 vasopressin receptor against polycystic kidney disease

2017 ◽  
Vol 114 (27) ◽  
pp. 7154-7159 ◽  
Author(s):  
Justyna Ciolek ◽  
Helen Reinfrank ◽  
Loïc Quinton ◽  
Say Viengchareun ◽  
Enrico A. Stura ◽  
...  
Keyword(s):  
Serine Proteases ◽  
Kidney Diseases ◽  
Genetic Disorders ◽  
Urine Osmolality ◽  
Ionic Channels ◽  
Vasopressin Receptor ◽  
Dependent Manner ◽  
Polycystic Kidney

Polycystic kidney diseases (PKDs) are genetic disorders that can cause renal failure and death in children and adults. Lowering cAMP in cystic tissues through the inhibition of the type-2 vasopressin receptor (V2R) constitutes a validated strategy to reduce disease progression. We identified a peptide from green mamba venom that exhibits nanomolar affinity for the V2R without any activity on 155 other G-protein–coupled receptors or on 15 ionic channels. Mambaquaretin-1 is a full antagonist of the V2R activation pathways studied: cAMP production, beta-arrestin interaction, and MAP kinase activity. This peptide adopts the Kunitz fold known to mostly act on potassium channels and serine proteases. Mambaquaretin-1 interacts selectively with the V2R through its first loop, in the same manner that aprotinin inhibits trypsin. Injected in mice, mambaquaretin-1 increases in a dose-dependent manner urine outflow with concomitant reduction of urine osmolality, indicating a purely aquaretic effect associated with the in vivo blockade of V2R. CD1-pcy/pcy mice, a juvenile model of PKD, daily treated with 13𝝁g of mambaquaretin-1 for 99 d, developed less abundant (by 33%) and smaller (by 47%) cysts than control mice. Neither tachyphylaxis nor apparent toxicity has been noted. Mambaquaretin-1 represents a promising therapeutic agent against PKDs.

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