P134. Cardiomyocyte-specific overexpression of nitric oxide synthase 3 improves left ventricular remodeling in mice with chronic pressure overload

Nitric Oxide ◽  
2006 ◽  
Vol 14 (4) ◽  
pp. 61-62
Author(s):  
Emmanuel S. Buys ◽  
Davinder S. Jassal ◽  
Tom G. Neilan ◽  
Michael J. Raher ◽  
Fumito Ichinose ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Nitric Oxide Synthase 3 ◽  
Oxide Synthase

scholarly journals Endothelial Nitric Oxide Synthase Limits Left Ventricular Remodeling After Myocardial Infarction in Mice

Circulation ◽  
2001 ◽  
Vol 104 (11) ◽  
pp. 1286-1291 ◽  
Author(s):  
Marielle Scherrer-Crosbie ◽  
Roman Ullrich ◽  
Kenneth D. Bloch ◽  
Hiroshi Nakajima ◽  
Boris Nasseri ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Myocardial Infarction ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Cardiomyocyte-restricted restoration of nitric oxide synthase 3 attenuates left ventricular remodeling after chronic pressure overload

2007 ◽  
Vol 293 (1) ◽  
pp. H620-H627 ◽  
Author(s):  
Emmanuel S. Buys ◽  
Michael J. Raher ◽  
Sarah L. Blake ◽  
Tomas G. Neilan ◽  
Amanda R. Graveline ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Ventricular Remodeling ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Cardiac Response ◽  
Lv Remodeling ◽  
And Function ◽  
Oxide Synthase ◽  
Deficient Mice

Although nitric oxide synthase (NOS)3 is implicated as an important modulator of left ventricular (LV) remodeling, its role in the cardiac response to chronic pressure overload is controversial. We examined whether selective restoration of NOS3 to the hearts of NOS3-deficient mice would modulate the LV remodeling response to transverse aortic constriction (TAC). LV structure and function were compared at baseline and after TAC in NOS3-deficient (NOS3−/−) mice and NOS3−/− mice carrying a transgene directing NOS3 expression specifically in cardiomyocytes (NOS3−/−TG mice). At baseline, echocardiographic assessment of LV dimensions and function, invasive hemodynamic measurements, LV mass, and myocyte width did not differ between the two genotypes. Four weeks after TAC, echocardiographic and hemodynamic indexes of LV systolic function indicated that contractile performance was better preserved in NOS3−/−TG mice than in NOS3−/− mice. Echocardiographic LV wall thickness and cardiomyocyte width were greater in NOS3−/− mice than in NOS3−/−TG mice. TAC-induced cardiac fibrosis did not differ between these genotypes. TAC increased cardiac superoxide generation in NOS3−/−TG but not NOS3−/− mice. The ratio of NOS3 dimers to monomers did not differ before and after TAC in NOS3−/−TG mice. Restoration of NOS3 to the heart of NOS3-deficient mice attenuates LV hypertrophy and dysfunction after TAC, suggesting that NOS3 protects against the adverse LV remodeling induced by prolonged pressure overload.

Nitric oxide synthase 2 and pressure-overload-induced left ventricular remodelling in mice

2006 ◽  
Vol 91 (3) ◽  
pp. 633-639 ◽  
Author(s):  
Ryuji Hataishi ◽  
Ana Clara Rodrigues ◽  
John G. Morgan ◽  
Fumito Ichinose ◽  
Geneviève Derumeaux ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Ventricular Remodelling ◽  
Left Ventricular Remodelling ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase
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