Mineralocorticoid receptor activation in myocardial infarction and failure: recent advances

Eur J Clin Invest. 2012 Oct;42(10):1112-20. doi: 10.1111/j.1365-2362.2012.02676.x. Epub 2012 Apr 26.

Abstract

The classical view of aldosterone actions via the mineralocorticoid receptor (MR) limited to control of fluid balance and blood pressure homoeostasis has been progressively overcome by clinical and experimental evidence emphasizing the pleiotropic role of MR activation in the pathogenesis of cardiovascular disease. Clinical studies have shown the benefit of MR blockade in patients with left ventricular dysfunction and heart failure after myocardial infarction (MI), hypertension or diabetic nephropathy. Deleterious effects of MR activation include cardiac structural and electrical remodelling, cardiovascular fibrosis, inflammation and oxidative stress. Complexity of pathophysiological role of MR derives from the presence of circulating glucocorticoids at higher concentrations than aldosterone and the equal affinity of the MR for aldosterone, cortisol and corticosterone. Recent experimental studies using different animal models and genetic tools have deeply explored the cell-specific functional role of MR in cardiovascular pathology. This review addresses emerging preclinical studies as well as ongoing clinical trials regarding MR activation in MI and failure.

Publication types

  • Review

MeSH terms

  • Aldosterone / physiology
  • Genetic Techniques
  • Heart Failure / etiology*
  • Humans
  • Hyperkalemia / chemically induced
  • Mineralocorticoid Receptor Antagonists / pharmacology
  • Mineralocorticoid Receptor Antagonists / therapeutic use
  • Myocardial Infarction / etiology*
  • Randomized Controlled Trials as Topic
  • Receptors, Mineralocorticoid / genetics
  • Receptors, Mineralocorticoid / metabolism*
  • Ventricular Dysfunction, Left / etiology

Substances

  • Mineralocorticoid Receptor Antagonists
  • Receptors, Mineralocorticoid
  • Aldosterone