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dc.contributor.author
Brocca, María Elvira
dc.contributor.author
Pietranera, Luciana
dc.contributor.author
De Kloet, Edo Ronald
dc.contributor.author
de Nicola, Alejandro Federico
dc.date.available
2020-12-09T20:53:40Z
dc.date.issued
2019-05
dc.identifier.citation
Brocca, María Elvira; Pietranera, Luciana; De Kloet, Edo Ronald; de Nicola, Alejandro Federico; Mineralocorticoid Receptors, Neuroinflammation and Hypertensive Encephalopathy; Springer/Plenum Publishers; Cellular And Molecular Neurobiology.; 39; 4; 5-2019; 483-492
dc.identifier.issn
0272-4340
dc.identifier.uri
http://hdl.handle.net/11336/120064
dc.description.abstract
Worldwide, raised blood pressure is estimated to affect 35–40% of the adult population and is a main conditioning factor for cardiovascular diseases and stroke. Animal models of hypertension have provided great advances concerning the pathophysiology of human hypertension, as already shown for the deoxycorticosterone-salt treated rat, the Dahl-salt sensitive rat, the Zucker obese rat and the spontaneously hypertensive rat (SHR). SHR has been widely used to study abnormalities of the brain in chronic hypertension. This review summarises present and past evidence that in the SHR, hypertension causes hippocampal tissue damage which triggers a pro-inflammatory feedforward cascade affecting this vulnerable brain region. The cascade is driven by mineralocorticoid receptor (MR) activation responding to endogenous corticosterone rather than aldosterone. Increased MR expression is a generalised feature of the SHR which seems to support first the rise in blood pressure. Then oxidative stress caused by vasculopathy and hypoxia further increases MR activation in hippocampal neurons and glia cells, activates microglia activation and pro-inflammatory mediators, and down-regulates anti-inflammatory factors. In contrast to MR, involvement of the glucocorticoid receptor (GR) in SHR is less certain. GR showed normal expression levels and blockage with an antagonist failed to reduce blood pressure of SHR. The findings support the concept that MR:GR imbalance caused by vasculopathy causes a switch in MR function towards a proverbial “death” receptor.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Springer/Plenum Publishers
dc.rights
info:eu-repo/semantics/restrictedAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
HYPERTENSION
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MICROGLIA
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MINERALOCORTICOID RECEPTOR
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NEUROINFLAMMATION
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Neurociencias
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Medicina Básica
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CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Mineralocorticoid Receptors, Neuroinflammation and Hypertensive Encephalopathy
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2020-11-17T18:30:55Z
dc.journal.volume
39
dc.journal.number
4
dc.journal.pagination
483-492
dc.journal.pais
Estados Unidos
dc.journal.ciudad
New York
dc.description.fil
Fil: Brocca, María Elvira. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Consejo Superior de Investigaciones Cientificas. Centro de Ciencias Humanas y Sociales. Instituto de Historia.; España
dc.description.fil
Fil: Pietranera, Luciana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Farmacologia; Argentina
dc.description.fil
Fil: De Kloet, Edo Ronald. Leiden University. Leiden University Medical Center.; Países Bajos
dc.description.fil
Fil: de Nicola, Alejandro Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Farmacologia; Argentina
dc.journal.title
Cellular And Molecular Neurobiology.
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://link.springer.com/10.1007/s10571-018-0610-9
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1007/s10571-018-0610-9
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