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Current Hypertension Reports

Erschienen in:

01.12.2018 | Inflammation and Cardiovascular Diseases (A Kirabo, Section Editor)

Inflammation in Salt-Sensitive Hypertension and Renal Damage

verfasst von: Xiaohan Lu, Steven D. Crowley

Erschienen in: Current Hypertension Reports | Ausgabe 12/2018

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Abstract

Purpose of Review

Low-grade inflammation drives elevations in blood pressure (BP) and consequent target organ damage in diverse experimental models of hypertension. Here, we discuss recent advances elucidating immune-mediated mechanisms of BP elevation and associated target organ damage.

Recent Findings

Inflammatory mediators produced by immune cells or target organs act on the kidney, vasculature, skin, and nervous system to modulate hypertension. For example, cells of the innate immune system, including monocytes, neutrophils, and dendritic cells (DCs), can all promote BP elevation via actions in the vasculature and kidney. Macrophages expressing VEGF-C impact non-osmotic sodium storage in the skin that in turn regulates salt sensitivity. Within the adaptive immune system, activated T cells can secrete tumor necrosis factor-alpha (TNF-α), interleukin-17a (IL-17a), and interferon-gamma (IFN-γ), each of which has augmented BP and renal damage in pre-clinical models. Inversely, deficiency of IL-17a in mice blunts the hypertensive response and attenuates renal sodium retention via a serum- and glucocorticoid-regulated kinase 1 (SGK1)–dependent pathway. Linking innate and adaptive immune responses, dendritic cells activated by augmented extracellular sodium concentrations stimulate T lymphocytes to produce pro-hypertensive cytokines. By contrast, regulatory T cells (Tregs) can protect against hypertension and associated kidney injury.

Summary

Rodent studies reveal diverse mechanisms via which cells of the innate and adaptive immune systems drive blood pressure elevation by altering the inflammatory milieu in the kidney, vasculature, and brain.

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Titel: Inflammation in Salt-Sensitive Hypertension and Renal Damage
verfasst von: Xiaohan Lu
Steven D. Crowley
Publikationsdatum: 01.12.2018
Verlag: Springer US
Erschienen in: Current Hypertension Reports / Ausgabe 12/2018
Print ISSN: 1522-6417
Elektronische ISSN: 1534-3111
DOI: https://doi.org/10.1007/s11906-018-0903-x

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