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Aldosterone as a modulator of immunity: implications in the organ damage

Herrada, Andrés A.a; Campino, Carmenc; Amador, Cristián A.b; Michea, Luis F.b; Fardella, Carlos E.a,c; Kalergis, Alexis M.a,d

doi: 10.1097/HJH.0b013e32834a4c75

High plasmatic levels of aldosterone cause hypertension and contribute to progressive organ damage to the heart, vasculature, and kidneys. Recent studies have demonstrated a role for the immune system in these pathological processes. Aldosterone promotes an inflammatory state characterized by vascular infiltration of immune cells, reactive oxidative stress, and proinflammatory cytokine production. Further, cells of the adaptive immune system, such as T cells, seem to participate in the genesis of mineralocorticoid hormone-induced hypertension. In addition, the observation that aldosterone can promote CD4+ T-cell activation and Th17 polarization suggests that this hormone could contribute to the onset of autoimmunity. Here we discuss recent evidence supporting a significant involvement of the immune system, especially adaptive immunity, in the genesis of hypertension and organ damage induced by primary aldosteronism. In addition, possible new therapeutic approaches consisting of immunomodulator drugs to control exacerbated immune responses triggered by elevated aldosterone concentrations will be described.

aDepartamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Millennium Institute on Immunology and Immunotherapy, Pontificia Universidad Católica de Chile

bMillennium Institute on Immunology and Immunotherapy, Instituto de Ciencias Biomédicas, Centro de Estudios Moleculares de la Célula, Facultad de Medicina, Universidad de Chile

cDepartamento de Endocrinología

dDepartamento de Reumatología, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile

Correspondence to A.M. Kalergis, Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Portugal #49, Santiago, Chile Tel: +56 2 686 2842; fax: +56 2 686 2185; e-mail:

Abbreviations: Ang II, angiotensin-II; CCR2, chemokine receptor 2; DOCA, deoxycorticosterone acetate; EAE, experimental autoimmune encephalomyelitis; EPHESUS, Eplerenone Post-Acute Myocardial Infarction Heart and Survival Study; HE, hypertension patients; ICAM-1, intercellular adhesion molecule 1; IGF-IR, insulin-like growth factor-I receptors; LFA-1, lymphocyte function-associated antigen 1; MAPK, mitogen-activated protein kinase; MCP-1, monocyte chemoattractant protein 1; NADPHox, NADPH oxidase; NF-κB, nuclear factor-kappaB; OPN, osteopontin; PBMCs, peripheral blood mononuclear cells; RALES, The Randomized Aldactone Evaluation Study; ROS, reactive oxygen species; TGF-ß, transforming growth factor-ß VSMC, vascular smooth muscle cells

Received 24 January, 2011

Revised 23 May, 2011

Accepted 27 June, 2011

© 2011 Lippincott Williams & Wilkins, Inc.