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Aldosterone Contributes to Vasopressin Escape through Changes in Water and Urea Transport

Hyponatremia (hypo-osmolality) is a disorder of water homeostasis due to abnormal renal diluting capacity. The body limits the degree to which serum sodium concentration falls through a mechanism called “vasopressin escape”. Vasopressin escape is a process that prevents the continuous decrease in se...

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Autores principales: Wang, Yanhua, LaRocque, Lauren M., Ruiz, Joseph A., Rodriguez, Eva L., Sands, Jeff M., Klein, Janet D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10376660/
https://www.ncbi.nlm.nih.gov/pubmed/37509484
http://dx.doi.org/10.3390/biomedicines11071844
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author Wang, Yanhua
LaRocque, Lauren M.
Ruiz, Joseph A.
Rodriguez, Eva L.
Sands, Jeff M.
Klein, Janet D.
author_facet Wang, Yanhua
LaRocque, Lauren M.
Ruiz, Joseph A.
Rodriguez, Eva L.
Sands, Jeff M.
Klein, Janet D.
author_sort Wang, Yanhua
collection PubMed
description Hyponatremia (hypo-osmolality) is a disorder of water homeostasis due to abnormal renal diluting capacity. The body limits the degree to which serum sodium concentration falls through a mechanism called “vasopressin escape”. Vasopressin escape is a process that prevents the continuous decrease in serum sodium concentration even under conditions of sustained high plasma vasopressin levels. Previous reports suggest that aldosterone may be involved in the vasopressin escape mechanism. The abilities of aldosterone synthase (Cyp11b2) knockout and wild-type mice to escape from vasopressin were compared. Wild-type mice escaped while the aldosterone synthase knockout mice did not. Both the water channel aquaporin 2 (AQP2) and the urea transporter UT-A1 protein abundances were higher in aldosterone synthase knockout than in wild-type mice at the end of the escape period. Vasopressin escape was also blunted in rats given spironolactone, a mineralocorticoid receptor blocker. Next, the role of the phosphatase, calcineurin (protein phosphatase 2B, PP2B), in vasopressin escape was studied since aldosterone activates calcineurin in rat cortical collecting ducts. Tacrolimus, a calcineurin inhibitor, blunted vasopressin escape in rats compared with the control rats, increased UT-A1, AQP2, and pS256-AQP2, and decreased pS261-AQP2 protein abundances. Our results indicate that aldosterone regulates vasopressin escape through calcineurin-mediated protein changes in UT-A1 and AQP2.
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spelling pubmed-103766602023-07-29 Aldosterone Contributes to Vasopressin Escape through Changes in Water and Urea Transport Wang, Yanhua LaRocque, Lauren M. Ruiz, Joseph A. Rodriguez, Eva L. Sands, Jeff M. Klein, Janet D. Biomedicines Article Hyponatremia (hypo-osmolality) is a disorder of water homeostasis due to abnormal renal diluting capacity. The body limits the degree to which serum sodium concentration falls through a mechanism called “vasopressin escape”. Vasopressin escape is a process that prevents the continuous decrease in serum sodium concentration even under conditions of sustained high plasma vasopressin levels. Previous reports suggest that aldosterone may be involved in the vasopressin escape mechanism. The abilities of aldosterone synthase (Cyp11b2) knockout and wild-type mice to escape from vasopressin were compared. Wild-type mice escaped while the aldosterone synthase knockout mice did not. Both the water channel aquaporin 2 (AQP2) and the urea transporter UT-A1 protein abundances were higher in aldosterone synthase knockout than in wild-type mice at the end of the escape period. Vasopressin escape was also blunted in rats given spironolactone, a mineralocorticoid receptor blocker. Next, the role of the phosphatase, calcineurin (protein phosphatase 2B, PP2B), in vasopressin escape was studied since aldosterone activates calcineurin in rat cortical collecting ducts. Tacrolimus, a calcineurin inhibitor, blunted vasopressin escape in rats compared with the control rats, increased UT-A1, AQP2, and pS256-AQP2, and decreased pS261-AQP2 protein abundances. Our results indicate that aldosterone regulates vasopressin escape through calcineurin-mediated protein changes in UT-A1 and AQP2. MDPI 2023-06-27 /pmc/articles/PMC10376660/ /pubmed/37509484 http://dx.doi.org/10.3390/biomedicines11071844 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Wang, Yanhua
LaRocque, Lauren M.
Ruiz, Joseph A.
Rodriguez, Eva L.
Sands, Jeff M.
Klein, Janet D.
Aldosterone Contributes to Vasopressin Escape through Changes in Water and Urea Transport
title Aldosterone Contributes to Vasopressin Escape through Changes in Water and Urea Transport
title_full Aldosterone Contributes to Vasopressin Escape through Changes in Water and Urea Transport
title_fullStr Aldosterone Contributes to Vasopressin Escape through Changes in Water and Urea Transport
title_full_unstemmed Aldosterone Contributes to Vasopressin Escape through Changes in Water and Urea Transport
title_short Aldosterone Contributes to Vasopressin Escape through Changes in Water and Urea Transport
title_sort aldosterone contributes to vasopressin escape through changes in water and urea transport
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10376660/
https://www.ncbi.nlm.nih.gov/pubmed/37509484
http://dx.doi.org/10.3390/biomedicines11071844
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