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Am J Physiol Heart Circ Physiol 289: H586-H592, 2005. First published March 11, 2005; doi:10.1152/ajpheart.00474.2004
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Gender-specific patterns of left ventricular and myocyte remodeling following myocardial infarction in mice deficient in the angiotensin II type 1a receptor

Paul Bridgman,1 Mark A. Aronovitz,1 Rahul Kakkar,1 Michael I. Oliverio,4 Thomas M. Coffman,4 William M. Rand,3 Marvin A. Konstam,2 Michael E. Mendelsohn,1,2 and Richard D. Patten1,2

1Molecular Cardiology Research Institute and 2Division of Cardiology and 3Department of Biostatistics, Tufts-New England Medical Center, Boston, Massachusetts; and 4Division of Nephrology, Department of Medicine, Duke University and Durham Veterans Affairs Medical Center, Durham, North Carolina

Submitted 28 May 2004 ; accepted in final form 4 March 2005

Left ventricular (LV) remodeling after myocardial infarction (MI) results from hypertrophy of myocytes and activation of fibroblasts induced, in part, by ligand stimulation of the 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 MI or sham procedures; echocardiography and hemodynamic evaluation were performed 6 wk 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 indexes were also similar except for lower systolic blood pressure in the AT1aR-KO mice compared with wild-type mice. 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 with shams. Both male and female wild-type mice demonstrated higher atrial natriuretic peptide (ANP) levels after 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 after 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.

angiotensin II receptors; ventricular remodeling; myocyte; hypertrophy


Address for reprint requests and other correspondence: R. D. Patten, Molecular Cardiology Research Institute, New England Medical Center, Box 80, 750 Washington St., Boston, MA 02111 (E-mail: rpatten{at}tufts-nemc.org)




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