Nitric Oxide Mediates Benefits of Angiotensin II Type 2 Receptor Overexpression during Post-Infarct Remodeling

Christina M. Bove, Zequan Yang, Wesley D. Gilson, Frederick H. Epstein, Brent A. French, Stuart S. Berr, Sanford P. Bishop, Hiroaki Matsubara, Robert M. Carey, Christopher M. Kramer

Research output: Contribution to journalArticlepeer-review

39 Scopus citations


We hypothesized that nitric oxide (NO) mediates the benefits of cardiac angiotensin II type 2 (AT2-R) overexpression during postmyocardial infarction (post-MI) remodeling. Eleven wild-type (WT) C57BL/6 mice and 28 transgenic (TG) mice with AT2-R overexpression were studied by cardiac magnetic resonance imaging (CMR) at baseline and days 1 and 28 post-MI induced by left anterior descending artery occlusion and reperfusion. Sixteen TG mice were treated from day 1 through 28 post-MI with the NO synthase inhibitor NG-nitro-L-arginine methyl ester in drinking water at 1 mg/mL (TG-Rx). Left ventricular mass index (LVMI), end-diastolic volume index (EDVI) and end-systolic volume index (ESVI), wall thickness, percent thickening, and ejection fraction (EF) were measured. Infarct size on day 1 was assessed by post-contrast CMR. Interstitial collagen was quantified in noninfarcted regions. At baseline, heart rate (HR), blood pressure (BP), LVMI, EDVI, and ESVI were similar between groups, as were infarct size and weekly post-MI HR and systolic BP. By day 28 post-MI, EDVI and ESVI were similar in WT and TG-Rx, but significantly lower in TG (ESVI: 1.41±0.18 μL/g versus 2.53±0.14 μL/g in WT; 2.17±0.14 μL/g in TG-Rx; P2-R overexpression during post-MI remodeling.

Original languageEnglish (US)
Pages (from-to)680-685
Number of pages6
Issue number3
StatePublished - Mar 2004
Externally publishedYes


  • Angiotensin
  • Imaging
  • MRI
  • Myocardial infarction
  • Nitric oxide
  • Receptors
  • Remodeling

ASJC Scopus subject areas

  • Internal Medicine


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