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dc.contributor.authorAraos, Patricio
dc.contributor.authorFigueroa, Stefanny
dc.contributor.authorAmador, Cristián A.
dc.date.accessioned2020-11-23T21:12:43Z
dc.date.available2020-11-23T21:12:43Z
dc.date.issued2020-11-02
dc.identifier10.3390/ijms21228536
dc.identifier.issn16616596
dc.identifier.urihttps://hdl.handle.net/20.500.12728/7537
dc.description.abstractIt is well accepted that the immune system and some cells from adaptive and innate immunity are necessary for the initiation/perpetuation of arterial hypertension (AH). However, whether neutrophils are part of this group remains debatable. There is evidence showing that the neutrophil/lymphocyte ratio correlates with AH and is higher in non-dipper patients. On the other hand, the experimental neutrophil depletion in mice reduces basal blood pressure. Nevertheless, their participation in AH is still controversial. Apparently, neutrophils may modulate the microenvironment in blood vessels by increasing oxidative stress, favoring endothelial disfunction. In addition, neutrophils may contribute to the tissue infiltration of immune cells, secreting chemoattractant chemokines/cytokines and promoting the proinflammatory phenotype, leading to AH development. In this work, we discuss the potential role of neutrophils in AH by analyzing different mechanisms proposed from clinical and basic studies, with a perspective on cardiovascular and renal damages relating to the hypertensive phenotype.es_ES
dc.language.isoenes_ES
dc.publisherMDPI AGes_ES
dc.subjectHypertensiones_ES
dc.subjectInflammationes_ES
dc.subjectInnate immunityes_ES
dc.subjectNeutrophiles_ES
dc.subjectOxidative stresses_ES
dc.titleThe role of neutrophils in hypertensiones_ES
dc.typeArticlees_ES


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