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Am J Physiol Heart Circ Physiol (March 11, 2005). doi:10.1152/ajpheart.00474.2004
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Submitted on May 28, 2004
Accepted on March 4, 2005

Gender Specific Patterns of Left Ventricular and Myocyte Remodeling Following Myocardial Infarction in Mice Deficient in the Angiotensin II Type 1a Receptor

Paul Bridgman1, Mark A Aronovitz1, Rahul Kakkar1, Michael I Oliverio1, Thomas M Coffman1, William M Rand1, Marvin A Konstam1, Michael E Mendelsohn1, and Richard D Patten1*

1 Molecular Cardiology Research Institute, Tufts-New England Medical Center, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: rpatten{at}tufts-nemc.org.

Left ventricular (LV) remodeling following myocardial infarction (MI) results from hypertrophy of myocytes and activation of fibroblasts induced, in part, by ligand stimulation of the angiotensin II (Ang II) type 1 receptor (AT1R). The purpose of the present study was to explore the specific role for activation of the AT1aR subtype in post-MI remodeling and whether gender differences exist in the patterns of remodeling in wild type and AT1aR knockout (KO) mice. AT1aR-KO mice and wild type littermates underwent coronary ligation to induce myocardial infarction (MI) or sham procedure; echocardiography and hemodynamic evaluation were performed six weeks later and LV tissue was harvested for infarct size determination, morphometric measurements, and gene expression analysis. Survival and infarct size were similar among all male and female wild type and AT1aR-KO mice. Hemodynamic indices were also similar except for lower systolic blood pressure in the AT1aR-KO mice compared to wild types. Male and female wild type and male AT1aR-KO mice developed similar increases in LV chamber size, LV mass corrected for body weight (LV/BW) and myocyte cross sectional area (CSA). However, female AT1aR-KO mice demonstrated no increase in LV/BW and myocyte CSA post-MI compared to shams. Both male and female wild type mice demonstrated higher ANP levels following MI with female wild types being significantly greater than males. However, male and female AT1aR-KO mice developed no increase in ANP gene expression with MI despite an increase in LV mass and myocyte size in males. These data support that gender specific patterns of LV and myocyte hypertrophy exist following MI in mice with a disrupted AT1aR gene, and suggest that myocyte hypertrophy post-MI in females relies, in part, on activation of the AT1aR. Further work is necessary to explore the potential mechanisms underlying these gender-based differences.




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