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Angiotensin II type 1 receptor blocker attenuates diabetes-induced atrial structural remodeling

Takeshi Kato1, Takeshi Yamashita, Akiko Sekiguchi

  • 1The Cardiovascular Institute, Tokyo, Japan. takeshikato@me.com

Journal of Cardiology
|August 2, 2011
PubMed
Abstract

Insights

Candesartan treatment reduced fibrosis and connective tissue growth factor (CTGF) expression in the atria of diabetic rats. This suggests candesartan may protect against diabetes-related atrial arrhythmias.

Area of Science:

  • Cardiovascular Research
  • Endocrinology
  • Pharmacology

Background:

  • Diabetes mellitus contributes to atrial structural remodeling and arrhythmogenicity.
  • Advanced glycation endproducts (AGEs) and their receptor (RAGE) are implicated in diabetes-related atrial pathogenesis.

Purpose of the Study:

  • To investigate the effects of candesartan, an angiotensin II receptor blocker, on diabetes-induced atrial structural changes.
  • To evaluate candesartan's impact on fibrosis and related protein expressions in diabetic rat atria.

Main Methods:

  • Diabetes was induced in Sprague-Dawley rats using streptozotocin.
  • Candesartan was administered at a subdepressor dose (0.05 mg/kg/day) via osmotic pumps.
  • Atrial fibrosis, RAGE, and CTGF expressions were assessed 12 weeks post-induction.

Main Results:

  • Diabetic rats exhibited elevated blood glucose and HbA1c, unaffected by candesartan.
  • Diabetic atria showed significant interstitial fibrosis with increased RAGE and CTGF expression.
  • Candesartan treatment significantly reduced CTGF expression and attenuated fibrotic deposition.

Conclusions:

  • Candesartan effectively reduced CTGF expression and atrial fibrosis in diabetic rats.
  • These findings suggest a protective role for candesartan against diabetes-related atrial structural remodeling and potential arrhythmias.

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