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Aldosterone and the Mineralocorticoid Receptor: Risk Factors for Cardiometabolic Disorders

  • Hypertension and the Kidney (RM Carey, Section Editor)
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Abstract

Preclinical studies have convincingly demonstrated a role for the mineralocorticoid receptor (MR) in adipose tissue physiology. These studies show that increased MR activation causes adipocyte dysfunction leading to decreased production of insulin-sensitizing products and increased production of inflammatory factors, creating an environment conducive to metabolic and cardiovascular disease. Accumulating data also suggest that MR activation may be an important link between obesity and metabolic syndrome. Moreover, MR activation may mediate the pathogenic consequences of metabolic syndrome. Recent attempts at reversing cardiometabolic damage in patients with type 2 diabetes using MR antagonists have shown promising results. MR antagonists are already used to treat heart failure where their use decreases mortality and morbidity over and above the use of traditional therapies alone. However, more data are needed to establish the benefits of MR antagonists in diabetes, obesity, and metabolic syndrome.

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Acknowledgments

This work was supported in part by NIH grant K24 HL103845

Compliance with Ethics Guidelines

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Conflict of Interest

Gail K. Adler declares personal fees from Pfizer, Japan. Rajesh Garg declares no conflict of interest.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

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  1. Division of Endocrinology, Diabetes and Hypertension, Brigham and Women’s Hospital, Harvard Medical School, 221 Longwood Avenue, Boston, MA, 02115, USA

    Rajesh Garg & Gail K. Adler

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  1. Rajesh Garg
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Correspondence to Gail K. Adler.

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This article is part of the Topical Collection on Hypertension and the Kidney

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Garg, R., Adler, G.K. Aldosterone and the Mineralocorticoid Receptor: Risk Factors for Cardiometabolic Disorders. Curr Hypertens Rep 17, 52 (2015). https://doi.org/10.1007/s11906-015-0567-8

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  • DOI: https://doi.org/10.1007/s11906-015-0567-8

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