Brain inflammation and hypertension: the chicken or the egg?

Journal of Neuroinflammation

Urszula Demkow³  Magdalena Wszedybyl-Winklewska¹  Marek Radkowski²  Pawel J Winklewski¹ 

[1] Institute of Human Physiology, Medical University of Gdansk, Tuwima Str. 15, Gdansk, 80-210, Poland;Department of Immunopathology of Infectious and Parasitic Diseases, Medical University of Warsaw, Pawinskiego Str. 3c, Warsaw, 02-106, Poland;Department of Laboratory Diagnostics and Clinical Immunology of Developmental Age, Medical University of Warsaw, Marszalkowska Str. 24, Warsaw, 00-576, Poland

关键词: Obesity;    Chronic inflammation;    Reactive oxygen species;    Prorenin;    Angiotensin II;    Neurogenic hypertension;    Brain inflammation;   

Others  :  1213711
DOI  :  10.1186/s12974-015-0306-8

 received in 2015-02-27, accepted in 2015-04-23,  发布年份 2015

【 摘 要 】

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.

【 授权许可】

   
2015 Winklewski et al; licensee BioMed Central.

【 图 表 】

Figure 1.

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