The expression of RAC1 and mineralocorticoid pathway-dependent genes are associated with different responses to salt intake

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dc.contributor.authorTapia-Castillo, Alejandra
dc.contributor.authorCarvajal, Cristian A.
dc.contributor.authorCampino, Carmen
dc.contributor.authorHill, Caroline
dc.contributor.authorAllende, Fidel
dc.contributor.authorVecchiola, Andrea
dc.contributor.authorCarrasco, Carmen
dc.contributor.authorBancalari, Rodrigo
dc.contributor.authorValdivia, Carolina
dc.contributor.authorLagos, Carlos
dc.contributor.authorMartinez-Aguayo, Alejandro
dc.contributor.authorGarcia, Hernan
dc.contributor.authorAglony, Marlene
dc.contributor.authorBaudrand, Rene F.
dc.contributor.authorKalergis, Alexis M.
dc.contributor.authorMichea, Luis F.
dc.contributor.authorRiedel, Claudia A.
dc.contributor.authorFardella, Carlos E.
dc.date.accessioned2023-05-23T17:56:27Z
dc.date.available2023-05-23T17:56:27Z
dc.date.issued2015-06
dc.descriptionIndexación: Scopuses
dc.description.abstractBackground Rac1 upregulation has been implicated in salt-sensitive hypertension as a modulator of mineralocorticoid receptor (MR) activity. Rac1 could affect the expression of oxidative stress markers, such as hemoxigenase-1 (HO- 1) or nuclear factor-B (NF-κB), and the expression of neutrophil gelatinaseassociated lipocalin (NGAL), a cytokine upregulated upon MR activation. aim We evaluated RAC1 expression in relation of high salt intake and association with MR, NGAL, HO-1, and NF-κB expression, mineralo- and glucocorticoids levels, and inflammatory parameters. subjects and methods We studied 147 adult subjects. A food survey identified the dietary sodium (Na) intake. RAC1 expression was considered high or low according to the value found in normotensive subjects with low salt intake. We determined the gene expression of RAC1, MR, NGAL, HO-1, NF-κB, and 18S, isolated from peripheral leukocytes. We measured aldosterone, cortisol, sodium, potassium excretion, metalloproteinase (MMP9 y MMP2), and C-reactive protein. results We identified 126 subjects with high Na-intake, 18 subjects had high, and 108 low-RAC1 expression. The subjects with high-RAC1 expression showed a significant increase in MR (P = 0.0002), NGAL (P < 0.0001) HO-1 (P = 0.0004), and NF-κB (P < 0.0001) gene expression. We demonstrated an association between RAC1 expression and MR (Rsp 0.64; P < 0.0001), NGAL (Rsp 0.48; P < 0.0001), HO-1 (Rsp 0.53; P < 0.0001), and NF-κB (Rsp0.52; P < 0.0001). We did not identify any association between RAC1 and clinical or biochemical variables. conclusions RAC1 expression was associated with an increase in MR, NGAL, NF-κB, and HO-1 expression, suggesting that RAC1 could be a mediator of cardiovascular damage induced by sodium, and may also useful to identify subjects with different responses to salt intake. © American Journal of Hypertension, Ltd 2014. All rights reserved.es
dc.description.urihttps://academic-oup-com.recursosbiblioteca.unab.cl/ajh/article/28/6/722/2743321
dc.identifier.citationAmerican Journal of Hypertension Volume 28, Issue 6, Pages 722 - 7281 June 2015es
dc.identifier.doi10.1093/ajh/hpu224
dc.identifier.issn0895-7061
dc.identifier.urihttps://repositorio.unab.cl/xmlui/handle/ria/49902
dc.language.isoenes
dc.publisherOxford University Presses
dc.rights.licenseAtribución 4.0 Internacional (CC BY 4.0)
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/deed.es
dc.subjectBlood pressurees
dc.subjectEssential hypertensiones
dc.subjectGene expressiones
dc.subjectHypertensiones
dc.subjectPBMCes
dc.subjectRAC1es
dc.subjectSalt intakees
dc.titleThe expression of RAC1 and mineralocorticoid pathway-dependent genes are associated with different responses to salt intakees
dc.typeArtículoes
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