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Cardiomyocyte loss in experimental renal failure: prevention by ramipril

Kerstin Amann1, Karin Tyralla, Marie-Luise Gross

  • 1Department of Pathology, University of Erlangen, Erlangen, Germany. kerstin.amann@path.imed.uni-erlangen.de

Kidney International
|April 5, 2003
PubMed

Insights

Renal failure causes left ventricular hypertrophy (LVH) through increased cardiomyocyte size and number loss. Ramipril treatment, an angiotensin-converting enzyme (ACE) inhibitor, reversed these cardiac changes in experimental renal failure.

Area of Science:

  • Cardiology
  • Nephrology
  • Experimental Medicine

Background:

  • Left ventricular hypertrophy (LVH) is a key cardiac abnormality in renal failure, contributing to cardiac mortality.
  • The impact of renal failure on cardiomyocyte volume and number in LVH development remains uninvestigated.
  • The renin-angiotensin system (RAS) is a suspected contributor to LVH in renal failure.

Purpose of the Study:

  • To characterize cardiomyocyte volume and number in short-term experimental renal failure.
  • To investigate the effect of the angiotensin-converting enzyme (ACE) inhibitor ramipril on these cardiac parameters.

Main Methods:

  • Subtotal nephrectomy (SNX) or sham operation was performed on rats, with one SNX group receiving ramipril.
  • Hearts were analyzed using stereologic techniques after 8 weeks.
  • Cardiomyocyte morphology, volume, and number were assessed.

Main Results:

  • SNX rats showed significantly increased left ventricular (LV) weight and cardiomyocyte volume, along with decreased cardiomyocyte number.
  • These LVH-associated changes were accompanied by an increase in TUNEL-positive myocytes.
  • Ramipril treatment abrogated cardiomyocyte hypertrophy and loss, and prevented the increase in LV weight.

Conclusions:

  • LVH in renal failure involves both cardiomyocyte hypertrophy and cell loss.
  • The beneficial effects of ramipril suggest a role for the RAS in LVH pathogenesis, independent of blood pressure changes.
  • ACE inhibition may be a therapeutic strategy for mitigating cardiac remodeling in renal failure.
Abstract

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