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Published in: Journal of Neuroinflammation 1/2015

Open Access 01-12-2015 | Review

Brain inflammation and hypertension: the chicken or the egg?

Authors: Pawel J Winklewski, Marek Radkowski, Magdalena Wszedybyl-Winklewska, Urszula Demkow

Published in: Journal of Neuroinflammation | Issue 1/2015

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Abstract

Inflammation of forebrain and hindbrain nuclei controlling the sympathetic nervous system (SNS) outflow from the brain to the periphery represents an emerging concept of the pathogenesis of neurogenic hypertension. Angiotensin II (Ang-II) and prorenin were shown to increase production of reactive oxygen species and pro-inflammatory cytokines (interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α)) while simultaneously decreasing production of interleukin-10 (IL-10) in the paraventricular nucleus of the hypothalamus and the rostral ventral lateral medulla. Peripheral chronic inflammation and Ang-II activity seem to share a common central mechanism contributing to an increase in sympathetic neurogenic vasomotor tone and entailing neurogenic hypertension. Both hypertension and obesity facilitate the penetration of peripheral immune cells in the brain parenchyma. We suggest that renin-angiotensin-driven hypertension encompasses feedback and feedforward mechanisms in the development of neurogenic hypertension while low-intensity, chronic peripheral inflammation of any origin may serve as a model of a feedforward mechanism in this condition.
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Metadata
Title
Brain inflammation and hypertension: the chicken or the egg?
Authors
Pawel J Winklewski
Marek Radkowski
Magdalena Wszedybyl-Winklewska
Urszula Demkow
Publication date
01-12-2015
Publisher
BioMed Central
Published in
Journal of Neuroinflammation / Issue 1/2015
Electronic ISSN: 1742-2094
DOI
https://doi.org/10.1186/s12974-015-0306-8

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