scholarly journals A High-Lipid Diet Potentiates Left Ventricular Dysfunction in Nitric Oxide Synthase 3-Deficient Mice after Chronic Pressure Overload

2010 ◽  
Vol 140 (8) ◽  
pp. 1438-1444 ◽  
Author(s):  
Roien Ahmadie ◽  
Jon-Jon Santiago ◽  
Jonathan Walker ◽  
Tielan Fang ◽  
Khuong Le ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Ventricular Dysfunction ◽  
Pressure Overload ◽  
Left Ventricular ◽  
High Lipid ◽  
Nitric Oxide Synthase 3 ◽  
Oxide Synthase ◽  
High Lipid Diet ◽  
Deficient Mice

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

Left ventricular adaptation to chronic pressure overload induced by inhibition of nitric oxide synthase in rats

1998 ◽  
Vol 93 (3) ◽  
pp. 173-181 ◽  
Author(s):  
B.B. Matsubara ◽  
L.S. Matsubara ◽  
L.A.M. Zornoff ◽  
M. Franco ◽  
J.S. Janicki
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Oxide Synthase

Effects of sex differences on constitutive nitric oxide synthase expression and activity in response to pressure overload in rats

2007 ◽  
Vol 293 (5) ◽  
pp. H2650-H2658 ◽  
Author(s):  
Xavier Loyer ◽  
Patricia Oliviero ◽  
Thibaud Damy ◽  
Estelle Robidel ◽  
Françoise Marotte ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Sex Differences ◽  
Nitric Oxide Synthase ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Female Rats ◽  
Male Rats ◽  
Male And Female ◽  
Constitutive Nitric Oxide Synthase ◽  
Oxide Synthase

Clinical studies have documented sex differences in left ventricular (LV) hypertrophy patterns, but the mechanisms are so far poorly defined. This study aimed to determine whether 1) severe pressure overload altered expression and/or activity of cardiac constitutive nitric oxide synthase (NOS1 and NOS3) and 2) these changes were modulated according to sex. Analyses were performed 0.4–20 wk after thoracic aortic constriction (TAC) in male and female Wistar rats. Male rats with TAC exhibited early signs of cardiac dysfunction, as shown by echocardiographic and LV end-diastolic pressure measurements, whereas females with TAC exhibited higher LV hypertrophy (+96% vs. males at 20 wk; P < 0.05). After TAC, cardiac NOS1 expression was rapidly induced (0.4 wk) and stable afterward in males ( P < 0.05 vs. sham groups), whereas it was delayed in females. Accordingly, specific NOS1 activity was increased by 2 wk in male rats with TAC (+122%; P < 0.001 vs. sham groups) and only by 20 wk in females (+220%; P < 0.001 vs. sham groups). NOS1 activity was correlated with NOS1 level. Regarding cardiac NOS3, expression was unaffected by TAC, and the decrease in activity observed at early and late times in male and female rats with TAC, respectively, is shown to be related to NOS3 allosteric regulator caveolin-1 level. The data demonstrated a unique sex-dependent regulation of the constitutive NOSs in response to TAC in rats; such a difference might play a role in the sex-dependent adaptability of the heart in response to pressure overload.

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