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Caffeine intake antagonizes salt sensitive hypertension through improvement of renal sodium handling

High salt intake is a major risk factor for hypertension. Although acute caffeine intake produces moderate diuresis and natriuresis, caffeine increases the blood pressure (BP) through activating sympathetic activity. However, the long-term effects of caffeine on urinary sodium excretion and blood pr...

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Autores principales: Yu, Hao, Yang, Tao, Gao, Peng, Wei, Xing, Zhang, Hexuan, Xiong, Shiqiang, Lu, Zongshi, Li, Li, Wei, Xiao, Chen, Jing, Zhao, Yu, Arendshorst, William J., Shang, Qianhui, Liu, Daoyan, Zhu, Zhiming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4866033/
https://www.ncbi.nlm.nih.gov/pubmed/27173481
http://dx.doi.org/10.1038/srep25746
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author Yu, Hao
Yang, Tao
Gao, Peng
Wei, Xing
Zhang, Hexuan
Xiong, Shiqiang
Lu, Zongshi
Li, Li
Wei, Xiao
Chen, Jing
Zhao, Yu
Arendshorst, William J.
Shang, Qianhui
Liu, Daoyan
Zhu, Zhiming
author_facet Yu, Hao
Yang, Tao
Gao, Peng
Wei, Xing
Zhang, Hexuan
Xiong, Shiqiang
Lu, Zongshi
Li, Li
Wei, Xiao
Chen, Jing
Zhao, Yu
Arendshorst, William J.
Shang, Qianhui
Liu, Daoyan
Zhu, Zhiming
author_sort Yu, Hao
collection PubMed
description High salt intake is a major risk factor for hypertension. Although acute caffeine intake produces moderate diuresis and natriuresis, caffeine increases the blood pressure (BP) through activating sympathetic activity. However, the long-term effects of caffeine on urinary sodium excretion and blood pressure are rarely investigated. Here, we investigated whether chronic caffeine administration antagonizes salt sensitive hypertension by promoting urinary sodium excretion. Dahl salt-sensitive (Dahl-S) rats were fed with high salt diet with or without 0.1% caffeine in drinking water for 15 days. The BP, heart rate and locomotor activity of rats was analyzed and urinary sodium excretion was determined. The renal epithelial Na(+) channel (ENaC) expression and function were measured by in vivo and in vitro experiments. Chronic consumption of caffeine attenuates hypertension induced by high salt without affecting sympathetic nerve activity in Dahl-S rats. The renal α-ENaC expression and ENaC activity of rats decreased after chronic caffeine administration. Caffeine increased phosphorylation of AMPK and decrease α-ENaC expression in cortical collecting duct cells. Inhibiting AMPK abolished the effect of caffeine on α-ENaC. Chronic caffeine intake prevented the development of salt-sensitive hypertension through promoting urinary sodium excretion, which was associated with activation of renal AMPK and inhibition of renal tubular ENaC.
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spelling pubmed-48660332016-05-31 Caffeine intake antagonizes salt sensitive hypertension through improvement of renal sodium handling Yu, Hao Yang, Tao Gao, Peng Wei, Xing Zhang, Hexuan Xiong, Shiqiang Lu, Zongshi Li, Li Wei, Xiao Chen, Jing Zhao, Yu Arendshorst, William J. Shang, Qianhui Liu, Daoyan Zhu, Zhiming Sci Rep Article High salt intake is a major risk factor for hypertension. Although acute caffeine intake produces moderate diuresis and natriuresis, caffeine increases the blood pressure (BP) through activating sympathetic activity. However, the long-term effects of caffeine on urinary sodium excretion and blood pressure are rarely investigated. Here, we investigated whether chronic caffeine administration antagonizes salt sensitive hypertension by promoting urinary sodium excretion. Dahl salt-sensitive (Dahl-S) rats were fed with high salt diet with or without 0.1% caffeine in drinking water for 15 days. The BP, heart rate and locomotor activity of rats was analyzed and urinary sodium excretion was determined. The renal epithelial Na(+) channel (ENaC) expression and function were measured by in vivo and in vitro experiments. Chronic consumption of caffeine attenuates hypertension induced by high salt without affecting sympathetic nerve activity in Dahl-S rats. The renal α-ENaC expression and ENaC activity of rats decreased after chronic caffeine administration. Caffeine increased phosphorylation of AMPK and decrease α-ENaC expression in cortical collecting duct cells. Inhibiting AMPK abolished the effect of caffeine on α-ENaC. Chronic caffeine intake prevented the development of salt-sensitive hypertension through promoting urinary sodium excretion, which was associated with activation of renal AMPK and inhibition of renal tubular ENaC. Nature Publishing Group 2016-05-12 /pmc/articles/PMC4866033/ /pubmed/27173481 http://dx.doi.org/10.1038/srep25746 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Yu, Hao
Yang, Tao
Gao, Peng
Wei, Xing
Zhang, Hexuan
Xiong, Shiqiang
Lu, Zongshi
Li, Li
Wei, Xiao
Chen, Jing
Zhao, Yu
Arendshorst, William J.
Shang, Qianhui
Liu, Daoyan
Zhu, Zhiming
Caffeine intake antagonizes salt sensitive hypertension through improvement of renal sodium handling
title Caffeine intake antagonizes salt sensitive hypertension through improvement of renal sodium handling
title_full Caffeine intake antagonizes salt sensitive hypertension through improvement of renal sodium handling
title_fullStr Caffeine intake antagonizes salt sensitive hypertension through improvement of renal sodium handling
title_full_unstemmed Caffeine intake antagonizes salt sensitive hypertension through improvement of renal sodium handling
title_short Caffeine intake antagonizes salt sensitive hypertension through improvement of renal sodium handling
title_sort caffeine intake antagonizes salt sensitive hypertension through improvement of renal sodium handling
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4866033/
https://www.ncbi.nlm.nih.gov/pubmed/27173481
http://dx.doi.org/10.1038/srep25746
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