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Aldosterone and end-organ damage.

Nancy J Brown1

  • 1Division of Clinical Pharmacology, Departments of Medicine and Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-6602, USA. nancy.j.brown@vanderbilt.edu

Current Opinion in Nephrology and Hypertension
|April 12, 2005
PubMed
Summary

Aldosterone contributes to cardiovascular and kidney disease by increasing oxidative stress and inflammation. Mineralocorticoid receptor antagonism offers a promising therapeutic strategy to reduce mortality and disease progression.

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Area of Science:

  • Cardiovascular Medicine
  • Endocrinology
  • Nephrology

Background:

  • Aldosterone plays a key role in cardiovascular and renal homeostasis.
  • Recent advances have elucidated the molecular mechanisms underlying aldosterone's effects.

Purpose of the Study:

  • To review recent clinical studies on aldosterone's contribution to cardiovascular mortality, vascular dysfunction, and renal injury.
  • To highlight the molecular biology of aldosterone and its clinical implications.

Main Methods:

  • Review of recent clinical studies.
  • Analysis of molecular mechanisms in animal models and human patients.
  • Examination of mineralocorticoid receptor-dependent and -independent pathways.

Main Results:

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  • Mineralocorticoid receptor antagonism reduces mortality in heart failure and post-myocardial infarction.
  • Aldosterone induces oxidative stress, endothelial dysfunction, and inflammation via mineralocorticoid receptor.
  • Aldosterone also exerts rapid, nongenomic effects on vascular tone.
  • Aldosterone stimulates fibrosis in the heart and kidney, partly dependent on sodium and mineralocorticoid receptor.
  • Mineralocorticoid antagonism reduces extracellular matrix turnover, cardiac remodeling, and albuminuria in humans.

Conclusions:

  • Aldosterone drives oxidative stress, endothelial dysfunction, inflammation, and fibrosis in cardiovascular and renal systems.
  • Mineralocorticoid receptor antagonism is a validated therapeutic approach.
  • Further research into non-MR pathways and inflammation-to-fibrosis progression is needed for novel strategies.