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Immune mechanisms in arterial hypertension. Recent advances

Increasing evidence indicates that hypertension and hypertensive end-organ damage are not only mediated by hemodynamic injury. Inflammation also plays an important role in the pathophysiology and contributes to the deleterious consequences of this disease. Cells of the innate immune system including...

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Autores principales: Wenzel, Ulrich O., Ehmke, Heimo, Bode, Marlies
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8523494/
https://www.ncbi.nlm.nih.gov/pubmed/33394136
http://dx.doi.org/10.1007/s00441-020-03409-0
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author Wenzel, Ulrich O.
Ehmke, Heimo
Bode, Marlies
author_facet Wenzel, Ulrich O.
Ehmke, Heimo
Bode, Marlies
author_sort Wenzel, Ulrich O.
collection PubMed
description Increasing evidence indicates that hypertension and hypertensive end-organ damage are not only mediated by hemodynamic injury. Inflammation also plays an important role in the pathophysiology and contributes to the deleterious consequences of this disease. Cells of the innate immune system including monocyte/macrophages and dendritic cells can promote blood pressure elevation via effects mostly on kidney and vascular function. Moreover, convincing evidence shows that T and B cells from the adaptive immune system are involved in hypertension and hypertensive end-organ damage. Skin monocyte/macrophages, regulatory T cells, natural killer T cells, and myeloid-derived suppressor cells have been shown to exert blood pressure controlling effects. Sodium intake is undoubtedly indispensable for normal body function but can be detrimental when taken in excess of dietary requirements. Sodium levels also modulate the function of monocyte/macrophages, dendritic cells, and different T cell subsets. Some of these effects are mediated by changes in the microbiome and metabolome that can be found after high salt intake. Modulation of the immune response can reduce severity of blood pressure elevation and hypertensive end-organ damage in several animal models. The purpose of this review is to briefly summarize recent advances in immunity and hypertension as well as hypertensive end-organ damage.
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spelling pubmed-85234942021-11-04 Immune mechanisms in arterial hypertension. Recent advances Wenzel, Ulrich O. Ehmke, Heimo Bode, Marlies Cell Tissue Res Review Increasing evidence indicates that hypertension and hypertensive end-organ damage are not only mediated by hemodynamic injury. Inflammation also plays an important role in the pathophysiology and contributes to the deleterious consequences of this disease. Cells of the innate immune system including monocyte/macrophages and dendritic cells can promote blood pressure elevation via effects mostly on kidney and vascular function. Moreover, convincing evidence shows that T and B cells from the adaptive immune system are involved in hypertension and hypertensive end-organ damage. Skin monocyte/macrophages, regulatory T cells, natural killer T cells, and myeloid-derived suppressor cells have been shown to exert blood pressure controlling effects. Sodium intake is undoubtedly indispensable for normal body function but can be detrimental when taken in excess of dietary requirements. Sodium levels also modulate the function of monocyte/macrophages, dendritic cells, and different T cell subsets. Some of these effects are mediated by changes in the microbiome and metabolome that can be found after high salt intake. Modulation of the immune response can reduce severity of blood pressure elevation and hypertensive end-organ damage in several animal models. The purpose of this review is to briefly summarize recent advances in immunity and hypertension as well as hypertensive end-organ damage. Springer Berlin Heidelberg 2021-01-04 2021 /pmc/articles/PMC8523494/ /pubmed/33394136 http://dx.doi.org/10.1007/s00441-020-03409-0 Text en © The Author(s) 2020 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Review
Wenzel, Ulrich O.
Ehmke, Heimo
Bode, Marlies
Immune mechanisms in arterial hypertension. Recent advances
title Immune mechanisms in arterial hypertension. Recent advances
title_full Immune mechanisms in arterial hypertension. Recent advances
title_fullStr Immune mechanisms in arterial hypertension. Recent advances
title_full_unstemmed Immune mechanisms in arterial hypertension. Recent advances
title_short Immune mechanisms in arterial hypertension. Recent advances
title_sort immune mechanisms in arterial hypertension. recent advances
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8523494/
https://www.ncbi.nlm.nih.gov/pubmed/33394136
http://dx.doi.org/10.1007/s00441-020-03409-0
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