Activation of AQP2 water channels without vasopressin: therapeutic strategies for congenital nephrogenic diabetes insipidus

Clinical and Experimental Nephrology
Fumiaki Ando, Shinichi Uchida

Abstract

Congenital nephrogenic diabetes insipidus (NDI) is characterized by defective urine concentrating ability. Symptomatic polyuria is present from birth, even with normal release of the antidiuretic hormone vasopressin by the pituitary. Over the last two decades, the aquaporin-2 (AQP2) gene has been cloned and the molecular mechanisms of urine concentration have been gradually elucidated. Vasopressin binds to the vasopressin type II receptor (V2R) in the renal collecting ducts and then activates AQP2 phosphorylation and trafficking to increase water reabsorption from urine. Most cases of congenital NDI are caused by loss-of-function mutations to V2R, resulting in unresponsiveness to vasopressin. In this article, we provide an overview of novel therapeutic molecules of congenital NDI that can activate AQP2 by bypassing defective V2R signaling with a particular focus on the activators of the calcium and cAMP signaling pathways.

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Citations

Aug 27, 2019·Frontiers in Physiology·Stine Julie TingskovRikke Nørregaard
Jun 27, 2019·Scientific Reports·Tamami FujikiShinichi Uchida
Sep 29, 2019·Annual Review of Pharmacology and Toxicology·Pui W CheungDennis Brown
Feb 26, 2019·F1000Research·Marianna RanieriGiovanna Valenti
Aug 10, 2019·Nature Reviews. Disease Primers·Mirjam Christ-CrainAlan S Verkman
Apr 14, 2019·Journal of the American Society of Nephrology : JASN·Joseph G Verbalis

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Methods Mentioned

BETA
confocal microscopy

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