We are analyzing https://link.springer.com/article/10.1186/s12974-015-0306-8.

Title:
Brain inflammation and hypertension: the chicken or the egg? | Journal of Neuroinflammation
Description:
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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Keywords {🔍}

pubmed, article, google, scholar, hypertension, cas, central, brain, inflammation, angii, neurogenic, inflammatory, activation, angiotensin, expression, sympathetic, physiol, sns, cytokines, pvn, obesity, system, rvlm, neuroinflammation, proinflammatory, activity, chronic, response, nucleus, cells, tissue, bbb, microglia, prorenin, mechanism, model, increased, cell, role, nadph, increase, peripheral, development, hypothalamic, cardiovascular, res, production, tnfα, heart, microglial,

Topics {✒️}

renin-angiotensin-aldosterone-ouabain system mitogen-activated protein kinases slow-pressor ang-ii model nadph oxidase-dependent pathway brain nuclear factor-kappa nadph oxidase-dependent production high-fat diet-induced obesity bone marrow-derived monocytes tumor necrosis factor-alpha reactive oxygen species brain renin-angiotensin system central anti-inflammatory action nuclear factor-kappa bone marrow-derived cells renin-ang-ii system angiotensin ii-induced hypertension central nervous system article download pdf low-fat diet represent doca-salt-induced hypertension [6] attenuating leptin-induced decreases superoxide mediates sympathoexcitation improved human thbmec-based high-dose endotoxin triggering reduce ang-ii formation ang-ii-induced hypertension ang-ii-induced hypertension [28-30] blood-brain barrier phenotype central ang ii pre-existing hypertensive condition blood-borne tnf-alpha angiotensin-converting enzyme mrna obesity-related insulin resistance renin-angiotensin system ang-ii-induced increase ras-induced hypertension represents doca-salt mouse model blood-borne inflammatory cytokines lps-induced at1r activity slow-pressor dose lps ros-generating systems anti-inflammatory cytokine interleukin-10 induce cox-2-dependent neuroinflammation chronic systemic inflammation ang-ii-pretreated microglia ang-ii-infused mice lps-induced microglia activation ang-ii/at1r mechanism sympathetic nervous system angiotensin-induced hypertension

Questions {❓}

Brain inflammation and hypertension: the chicken or the egg?
Brain inflammation and hypertension: the chicken or the egg?
Is neurogenic hypertension related to vascular inflammation of the brainstem?
Neuroimmune communication in hypertension and obesity: a new therapeutic angle?

Schema {🗺️}

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         headline:Brain inflammation and hypertension: the chicken or the egg?
         description: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.
         datePublished:2015-05-03T00:00:00Z
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      headline:Brain inflammation and hypertension: the chicken or the egg?
      description: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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         Brain inflammation
         Neurogenic hypertension
         Angiotensin II
         Prorenin
         Reactive oxygen species
         Chronic inflammation
         Obesity
         Neurosciences
         Neurology
         Neurobiology
         Immunology
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      name:Department of Immunopathology of Infectious and Parasitic Diseases, Medical University of Warsaw, Warsaw, Poland
      name:Institute of Human Physiology, Medical University of Gdansk, Gdansk, Poland
      name:Department of Laboratory Diagnostics and Clinical Immunology of Developmental Age, Medical University of Warsaw, Warsaw, Poland

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