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Disturbed acid-base transport: an emerging cause of hypertension

Genome-wide association studies and physiological investigations have linked alterations in acid-base transporters to hypertension. Accordingly, Na(+)-coupled HCO(−)(3)-transporters, Na(+)/H(+)-exchangers, and anion-exchangers have emerged as putative mechanistic components in blood pressure disturb...

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Autores principales: Boedtkjer, Ebbe, Aalkjaer, Christian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3870919/
https://www.ncbi.nlm.nih.gov/pubmed/24399970
http://dx.doi.org/10.3389/fphys.2013.00388
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author Boedtkjer, Ebbe
Aalkjaer, Christian
author_facet Boedtkjer, Ebbe
Aalkjaer, Christian
author_sort Boedtkjer, Ebbe
collection PubMed
description Genome-wide association studies and physiological investigations have linked alterations in acid-base transporters to hypertension. Accordingly, Na(+)-coupled HCO(−)(3)-transporters, Na(+)/H(+)-exchangers, and anion-exchangers have emerged as putative mechanistic components in blood pressure disturbances. Even though hypertension has been studied extensively over the last several decades, the cause of the high blood pressure has in most cases not been identified. Renal, cardiovascular, and neuronal dysfunctions all seem to play a role in hypertension development but their relative importance and mutual interdependency are still being debated. Multiple functional and structural alterations have been described in patients and animals with hypertension but it is typically unclear whether they are causes or consequences of hypertension or represent mechanistically unrelated associations. Perturbed blood pressure regulation has been demonstrated in several animal models with disrupted expression of acid-base transporters; and reciprocally, disturbed acid-base transport function has been described in hypertensive individuals. In addition to regulating intracellular and extracellular pH, Na(+)-coupled HCO(−)(3)-transport, Na(+)/H(+)-exchange, and anion-exchange also contribute to water and electrolyte balance in cells and systemically. Since acid-base transporters are widely expressed, alterations in transport activities likely affect multiple cell and organ functions, and it is a significant challenge to determine the mechanisms linking perturbed acid-base transport function to hypertension. It is the purpose of this review to evaluate the current evidence for involvement of acid-base transporters in hypertension development and discuss the cellular and integrative mechanisms, which may link changes in acid-base transport to blood pressure disturbances.
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spelling pubmed-38709192014-01-07 Disturbed acid-base transport: an emerging cause of hypertension Boedtkjer, Ebbe Aalkjaer, Christian Front Physiol Physiology Genome-wide association studies and physiological investigations have linked alterations in acid-base transporters to hypertension. Accordingly, Na(+)-coupled HCO(−)(3)-transporters, Na(+)/H(+)-exchangers, and anion-exchangers have emerged as putative mechanistic components in blood pressure disturbances. Even though hypertension has been studied extensively over the last several decades, the cause of the high blood pressure has in most cases not been identified. Renal, cardiovascular, and neuronal dysfunctions all seem to play a role in hypertension development but their relative importance and mutual interdependency are still being debated. Multiple functional and structural alterations have been described in patients and animals with hypertension but it is typically unclear whether they are causes or consequences of hypertension or represent mechanistically unrelated associations. Perturbed blood pressure regulation has been demonstrated in several animal models with disrupted expression of acid-base transporters; and reciprocally, disturbed acid-base transport function has been described in hypertensive individuals. In addition to regulating intracellular and extracellular pH, Na(+)-coupled HCO(−)(3)-transport, Na(+)/H(+)-exchange, and anion-exchange also contribute to water and electrolyte balance in cells and systemically. Since acid-base transporters are widely expressed, alterations in transport activities likely affect multiple cell and organ functions, and it is a significant challenge to determine the mechanisms linking perturbed acid-base transport function to hypertension. It is the purpose of this review to evaluate the current evidence for involvement of acid-base transporters in hypertension development and discuss the cellular and integrative mechanisms, which may link changes in acid-base transport to blood pressure disturbances. Frontiers Media S.A. 2013-12-24 /pmc/articles/PMC3870919/ /pubmed/24399970 http://dx.doi.org/10.3389/fphys.2013.00388 Text en Copyright © 2013 Boedtkjer and Aalkjaer. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Physiology
Boedtkjer, Ebbe
Aalkjaer, Christian
Disturbed acid-base transport: an emerging cause of hypertension
title Disturbed acid-base transport: an emerging cause of hypertension
title_full Disturbed acid-base transport: an emerging cause of hypertension
title_fullStr Disturbed acid-base transport: an emerging cause of hypertension
title_full_unstemmed Disturbed acid-base transport: an emerging cause of hypertension
title_short Disturbed acid-base transport: an emerging cause of hypertension
title_sort disturbed acid-base transport: an emerging cause of hypertension
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3870919/
https://www.ncbi.nlm.nih.gov/pubmed/24399970
http://dx.doi.org/10.3389/fphys.2013.00388
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