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The renin-angiotensin-aldosterone system and vascular remodeling

Yao Sun1

  • 1Division of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA. yasun@utmem.edu

Congestive Heart Failure (Greenwich, Conn.)
|February 1, 2002
PubMed

Insights

The renin-angiotensin-aldosterone system (RAAS) contributes to cardiac fibrosis and ventricular dysfunction. Blocking RAAS hormones, angiotensin II and aldosterone, can prevent cardiac and renal fibrosis.

Area of Science:

  • Cardiovascular Science
  • Renal Physiology
  • Endocrinology

Background:

  • Cardiac fibrosis is linked to ventricular dysfunction.
  • The renin-angiotensin-aldosterone system (RAAS) is associated with adverse cardiac remodeling.
  • Angiotensin II and aldosterone play roles in vascular remodeling via local and systemic actions.

Purpose of the Study:

  • To investigate the role of the RAAS in cardiac and renal fibrosis.
  • To examine the effects of angiotensin II and aldosterone on structural remodeling.
  • To assess the efficacy of RAAS antagonists in preventing fibrosis.

Main Methods:

  • Infusion of angiotensin II and aldosterone in rats.
  • Assessment of perivascular fibrosis in cardiac and renal arteries.
  • Evaluation of RAAS receptor antagonists' effects on fibrosis.

Main Results:

  • Angiotensin II and aldosterone infusion induced perivascular fibrosis in heart and kidney vasculature.
  • Evidence suggests local RAAS activation contributes to vascular remodeling.
  • RAAS receptor antagonists attenuated cardiac and renal fibrosis.

Conclusions:

  • The RAAS is a key mediator of cardiac and renal fibrosis.
  • Targeting RAAS activation with antagonists offers a potential therapeutic strategy for fibrotic diseases.

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