We are analyzing https://link.springer.com/article/10.1007/s10571-009-9368-4.

Title:
Anti-Inflammatory Effects of Angiotensin Receptor Blockers in the Brain and the Periphery | Cellular and Molecular Neurobiology
Description:
In addition to regulating blood pressure, Angiotensin II (Ang II) exerts powerful pro-inflammatory effects in hypertension through stimulation of its AT1 receptors, most clearly demonstrated in peripheral arteries and in the cerebral vasculature. Administration of Ang II receptor blockers (ARBs) decreases hypertension-related vascular inflammation in peripheral organs. In rodent models of genetic hypertension, ARBs reverse the inflammation in the cerebral microcirculation. We hypothesized that ARBs could be effective in inflammatory conditions beyond hypertension. Our more recent studies, summarized here, indicate that this is indeed the case. We used the model of systemic administration of the bacterial endotoxin lipopolysaccharide (LPS). LPS produces a robust initial inflammatory reaction, the innate immune response, in peripheral organs and in the brain. Pretreatment with the ARB candesartan significantly diminishes the response to LPS, including reduction of pro-inflammatory cytokine release to the general circulation and decreased production and release of the pro-inflammatory adrenal hormone aldosterone. In addition, the ARB very significantly decreased the LPS-induced gene expression of pro-inflammatory cytokines and microglia activation in the brain. Our results demonstrate that AT1 receptor activity is essential for the unrestricted development of full-scale innate immune response in the periphery and in the brain. ARBs, due to their immune response-limiting properties, may be considered as therapeutically useful in a number of inflammatory diseases of the peripheral organs and the brain.
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Keywords {🔍}

google, scholar, pubmed, article, cas, receptor, angiotensin, brain, saavedra, rats, peripheral, dois, inflammation, lipopolysaccharide, cell, physiol, lps, innate, expression, rat, effects, cerebral, administration, inflammatory, immune, hypertensive, blockade, res, system, pavel, blood, proinflammatory, hypertension, receptors, response, activation, antagonist, mol, health, neurobiol, research, benicky, vascular, stroke, factor, stress, sci, quan, disease, privacy,

Topics {✒️}

cold-restraint stress-induced increase month download article/chapter hypothalamic-pituitary-adrenal axis activity blood–brain barrier-independent pathways rat hypothalamo-pituitary-adrenal axis angiotensin-ii receptor subtypes at1 receptor antagonism renin-angiotensin system cytokine-induced sickness behavior receptor antagonist decreases nf-κb/iκb system hypothalamic-pituitary-adrenal response lps-induced gene expression pro-inflammatory cytokine mrnas isolation stress-induced decrease immune response-limiting properties brain-immune communications pathways at1 receptor activity pro-inflammatory cytokine release pro-inflammatory il-1β full article pdf anti-inflammatory il-10 cytokines at1 receptor antagonists angiotensin receptor blockers circulating inflammatory mediators central nervous system limiting inflammatory responses privacy choices/manage cookies brain angiotensin ii signaling cascades induced pro-inflammatory cytokines anti-inflammatory effects receptor 4-dependent pathway cortical crf1 receptor molecular neurobiology aims endotoxin-induced uveitis lps-induced production bacterial endotoxin lipopolysaccharide innate immune response alpha il-1β regulating blood pressure cerebral blood flow cns triggers neurodegeneration repeated immune challenge intramural research programs targeting bacterial endotoxin rel/nf-kappa tissue cytokine expression article cellular inflammatory signaling molecules

Questions {❓}

Neuroprotective effects of AT1 receptor antagonists after experimental ischemic stroke: what is important?
Quan N (2008) Immune-to-brain signaling: how important are the blood–brain barrier-independent pathways?
Rogers J, Mastroeni D, Leonard B, Joyce J, Grover A (2007) Neuroinflammation in Alzheimer’s disease and Parkinson’s disease: are microglia pathogenic in either disorder?
Singh AK, Jiang Y (2004) How does peripheral lipopolysaccharide induce gene expression in the brain of rats?

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