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Aldosterone antagonism fails to attenuate age-associated left ventricular fibrosis

Hyun Seok Hwang1, Georgina Cirrincione, D Paul Thomas

  • 1Division of Kinesiology, Laboratory of Molecular Kinesiology, University of Michigan, Ann Arbor, MI 48109-2214, USA.

The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
|April 25, 2007
PubMed

Insights

Spironolactone did not reduce age-related collagen buildup in rat hearts. This aldosterone antagonist did not prevent the natural increase in cardiac collagen with aging.

Area of Science:

  • Cardiovascular Physiology
  • Aging Research
  • Pharmacology

Background:

  • Collagen accumulation in the heart is linked to aging and hypertension.
  • Spironolactone, an aldosterone antagonist, can reduce collagen in hypertensive hearts.

Purpose of the Study:

  • To investigate if spironolactone can attenuate age-associated increases in cardiac collagen.
  • To determine the effect of chronic aldosterone antagonism on age-related cardiac remodeling.

Main Methods:

  • Female Fisher 344 rats of three age groups (3, 12, and 21 months) were treated with spironolactone or vehicle for two months.
  • Cardiac tissue was analyzed using immunoblotting, RNA blotting, and biochemical assays to quantify collagen and gene expression.

Main Results:

  • The oldest rats exhibited the highest percentage of collagen in the left ventricle and septum.
  • Spironolactone treatment did not significantly reduce the age-associated increase in collagen fraction.
  • Key gene markers for cardiac remodeling (atrial natriuretic factor and beta-myosin heavy chain) were not significantly affected by spironolactone in aged rats.

Conclusions:

  • Chronic aldosterone antagonism with spironolactone does not attenuate the age-associated increase in cardiac collagen fraction in female Fisher 344 rats.
  • The findings suggest that aldosterone antagonism may not be a viable strategy for preventing age-related cardiac fibrosis.

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