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Endogenous angiotensin-(1-7) reduces cardiac ischemia-induced dysfunction in diabetic hypertensive rats

May Al-Maghrebi1, Ibrahim F Benter, Debra I Diz

  • 1Department of Biochemistry, Faculty of Medicine, Kuwait University, Kuwait.

Pharmacological Research
|January 27, 2009
PubMed

Insights

Angiotensin-(1-7) peptide protects the heart from damage caused by ischemia/reperfusion in diabetic rats. This effect involves reducing inflammation and is linked to the peptide

Area of Science:

  • Cardiovascular Pharmacology
  • Renal Physiology
  • Molecular Cardiology

Background:

  • Angiotensin-(1-7) [Ang-(1-7)] is a vasoactive peptide with demonstrated cardiac and vascular protective effects.
  • Diabetic spontaneously hypertensive rats (SHR) exhibit exacerbated cardiac dysfunction following ischemia/reperfusion (I/R) injury.
  • The role of endogenous Ang-(1-7) and the mechanisms underlying its cardioprotective effects in diabetes remain incompletely understood.

Purpose of the Study:

  • To investigate the influence of endogenous and exogenously administered Ang-(1-7) on I/R-induced cardiac dysfunction in diabetic SHR.
  • To explore the impact of Ang-(1-7) on cardiac NF-kappaB activity and inflammatory gene expression in this model.
  • To elucidate the contribution of the Ang-(1-7) receptor (AT((1-7))) to the observed cardioprotective effects.

Main Methods:

  • Isolated perfused hearts from streptozotocin-treated diabetic SHR subjected to 40 minutes of global ischemia followed by reperfusion.
  • Chronic administration of Ang-(1-7) or captopril, with or without the AT((1-7)) antagonist A779.
  • Assessment of left ventricular function recovery, cardiac NF-kappaB activity, and gene expression profiling using real-time PCR arrays.

Main Results:

  • Treatment with Ang-(1-7) or captopril significantly improved recovery of left ventricular function post-I/R in diabetic SHR.
  • Administration of A779 worsened cardiac recovery and partially reversed the beneficial effects of captopril and Ang-(1-7).
  • Ang-(1-7) and captopril treatment reduced elevated cardiac NF-kappaB activity and decreased the expression of inflammatory genes, an effect partially blocked by A779.

Conclusions:

  • Endogenous Ang-(1-7) plays a protective role against I/R-induced cardiac dysfunction in diabetic SHR.
  • Exogenous Ang-(1-7) administration confers significant cardioprotection in this model, likely mediated through anti-inflammatory pathways involving NF-kappaB.
  • The findings confirm the therapeutic potential of Ang-(1-7) for managing cardiac complications in diabetes.

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