Cardiac Angiotensin-(1-7) in Ischemic Cardiomyopathy

DOI Web Site 4 Citations
  • David B. Averill
    From The Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Winston-Salem, NC.
  • Yuichiro Ishiyama
    From The Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Winston-Salem, NC.
  • Mark C. Chappell
    From The Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Winston-Salem, NC.
  • Carlos M. Ferrario
    From The Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Winston-Salem, NC.

Abstract

<jats:p> <jats:bold> <jats:italic>Background—</jats:italic> </jats:bold> Accumulating evidence suggests that angiotensin-(1-7) (Ang-[1-7]) may play an important role in counteracting the pressor, proliferative, and profibrotic actions of angiotensin II in the heart. Thus, we evaluated whether Ang-(1-7) is expressed in the myocardium of normal rats and those in which myocardial infarction was produced 4 weeks beforehand. </jats:p> <jats:p> <jats:bold> <jats:italic>Methods and Results—</jats:italic> </jats:bold> The left coronary artery in 10-week-old Lewis rats was either ligated (n=5) or exposed but not occluded in age-matched controls (sham; n=5). Left ventricular end-diastolic pressures were significantly elevated 4 weeks after myocardial infarction (25±1 versus 5±1 mm Hg for sham; <jats:italic>P</jats:italic> <0.001), whereas left ventricular systolic pressures were significantly reduced (ligated 86±4 versus sham 110±5 mm Hg; <jats:italic>P</jats:italic> <0.01). Hemodynamic effects of coronary artery ligation were accompanied by significant cardiac hypertrophy (heart weight to body weight: ligated 4.3±0.1 versus sham 2.9±0.1 mg/g; <jats:italic>P</jats:italic> <0.001). In both ligated and sham rats, Ang-(1-7) immunoreactivity was limited to cardiac myocytes and absent in interstitial cells and coronary vessels. Ang-(1-7) immunoreactivity was significantly augmented in ventricular tissue surrounding the infarct area in the heart of rats with myocardial infarction. </jats:p> <jats:p> <jats:bold> <jats:italic>Conclusions—</jats:italic> </jats:bold> Development of heart failure subsequent to coronary artery ligation leads to increased expression of Ang-(1-7),which was restricted to myocytes. </jats:p>

Journal

  • Circulation

    Circulation 108 (17), 2141-2146, 2003-10-28

    Ovid Technologies (Wolters Kluwer Health)

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