Cardiomyocyte-specific Nitric Oxide Synthase 3 Overexpression in Pressure-Overloaded Left Ventricle.

ABSTRACT: Aims: Cardiomyocyte-specific nitric oxide synthase 3 (NOS3) overexpression reduces left ventricular (LV) remodelling after myocardial infarction in mice, but its effect on sustained LV pressure-overload remains incompletely understood. We investigated LV structural and functional adaptation to elevated afterload in mice with cardiomyocyte-restricted NOS3 overexpression (NOS3TG) and wild type littermates (WT). Methods and Results: Hemodynamic indices, cardiac hypertrophy and interstitial fibrosis were measured 10 weeks after transverse aortic constriction (TAC). After 10 weeks TAC, NOS3TG had better preserved systolic function (maximum rates of pressure development normalized to maximal pressure 77±6 versus 65±2 ms-1, P=0.05), reduced heart weight-body weight ratio (HW/BW, 5.0±0.3 versus

ORGANISM(S): Mus musculus

SUBMITTER: Wouter Van Delm 

PROVIDER: E-GEOD-37597 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress