Winklewski Pawel J, Radkowski Marek, Wszedybyl-Winklewska Magdalena, Demkow Urszula
Institute of Human Physiology, Medical University of Gdansk, Tuwima Str. 15, 80-210, Gdansk, Poland.
Department of Immunopathology of Infectious and Parasitic Diseases, Medical University of Warsaw, Pawinskiego Str. 3c, 02-106, Warsaw, Poland.
J Neuroinflammation. 2015 May 3;12:85. doi: 10.1186/s12974-015-0306-8.
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.
控制从大脑到外周的交感神经系统（SNS）传出的前脑和后脑核的炎症代表了神经源性高血压发病机制的一个新出现的概念。已表明血管紧张素II（Ang-II）和肾素原可增加活性氧和促炎细胞因子（白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α））的产生，同时降低下丘脑室旁核和延髓头端腹外侧中白细胞介素-10（IL-10）的产生。外周慢性炎症和Ang-II活性似乎共享一种共同的中枢机制，导致交感神经源性血管运动张力增加并引发神经源性高血压。高血压和肥胖都促进外周免疫细胞穿透脑实质。我们认为，肾素-血管紧张素驱动的高血压在神经源性高血压的发展中包含反馈和前馈机制，而任何来源的低强度慢性外周炎症都可能作为这种情况下前馈机制的一个模型。
