Back to Search
Start Over
Gender-specific patterns of left ventricular and myocyte remodeling following myocardial infarction in mice deficient in the angiotensin II type 1a receptor
- Source :
- The American Journal of Physiology. August, 2005, Vol. 289 Issue 2, pH586, 7 p.
- Publication Year :
- 2005
-
Abstract
- 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 (A[T.sub.1]R). The purpose of the present study was to explore the specific role for activation of the A[T.sub.1a]R subtype in post-MI remodeling and whether gender differences exist in the patterns of remodeling in wild-type and A[T.sub.1a]R knockout (KO) mice. A[T.sub.1a]R-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 A[T.sub.1a]R-KO mice. Hemodynamic indexes were also similar except for lower systolic blood pressure in the A[T.sub.1a]R-KO mice compared with wild-type mice. Male and female wild-type and male A[T.sub.1a]R-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 A[T.sub.1a]R-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 A[T.sub.1a]R-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 A[T.sub.1a]R gene, and suggest that myocyte hypertrophy post-MI in females relies, in part, on activation of the A[T.sub.1a]R. Further work is necessary to explore the potential mechanisms underlying these gender-based differences. angiotensin II receptors; ventricular remodeling; myocyte; hypertrophy
Details
- Language :
- English
- ISSN :
- 00029513
- Volume :
- 289
- Issue :
- 2
- Database :
- Gale General OneFile
- Journal :
- The American Journal of Physiology
- Publication Type :
- Academic Journal
- Accession number :
- edsgcl.135245187