scholarly journals Overexpression of Endothelial Nitric Oxide Synthase Attenuates Cardiac Hypertrophy Induced by Chronic Isoproterenol Infusion

2002 ◽  
Vol 66 (9) ◽  
pp. 851-851 ◽  
Author(s):  
Masanori Ozaki ◽  
Seinosuke Kawashima ◽  
Tomoya Yamashita ◽  
Tetsuaki Hirase ◽  
Yoshitaka Ohashi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cardiac Hypertrophy ◽  
Endothelial Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Isoproterenol Infusion

Endothelial Nitric Oxide Synthase Haplotypes Associated with Hypertension Do Not Predispose to Cardiac Hypertrophy

2010 ◽  
Vol 29 (4) ◽  
pp. 171-176 ◽  
Author(s):  
Vivian Vasconcellos ◽  
Riccardo Lacchini ◽  
Anna L.B. Jacob-Ferreira ◽  
Maria L. Sales ◽  
Maria C. Ferreira-Sae ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cardiac Hypertrophy ◽  
Endothelial Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

scholarly journals Compensated cardiac hypertrophy in endothelial nitric oxide synthase knockout mice

2002 ◽  
Vol 39 ◽  
pp. 131
Author(s):  
Michael P. Flaherty ◽  
Maria Brown ◽  
Hitoshi Takano ◽  
Ingrid L. Grupp ◽  
Jo El Schultz ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cardiac Hypertrophy ◽  
Knockout Mice ◽  
Endothelial Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Increased expression of endothelial nitric oxide synthase and caveolin-1 in the aorta of rats with isoproterenol-induced cardiac hypertrophy

2006 ◽  
Vol 84 (12) ◽  
pp. 1245-1250 ◽  
Author(s):  
P. Krenek ◽  
J. Klimas ◽  
M. Kroslakova ◽  
A. Gazova ◽  
J. Plandorova ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Function ◽  
Cardiac Hypertrophy ◽  
Sodium Nitroprusside ◽  
Endothelial Nitric Oxide Synthase ◽  
Caveolin 1 ◽  
Isolated Aorta ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Isoproterenol-induced cardiac hypertrophy is associated with increased expression of endothelial nitric oxide synthase in the aorta but without signs of improved endothelial function. The aim was to examine the hypothesis that increased expression of eNOS allosteric inhibitor caveolin-1 could be associated with unimproved endothelium-dependent relaxations. Rats received isoproterenol (5 mg/kg body mass, i.p., n = 13) or its vehicle (n = 14) during 1 week. Systolic blood pressure (SBP) and heart rate (HR) were measured by the tail-cuff method. Expression of eNOS and caveolin-1 was measured using immunoblotting analysis. Relaxations of isolated aorta to acetylcholine and sodium nitroprusside were evaluated ex vivo. After 1 week of isoproterenol administration, basal SBP and HR were decreased (SBP 110 ± 3 vs. 126 ± 3 mmHg, p < 0.05; HR 342 ± 8 vs. 366 ± 6 beats/min, p < 0.05). Isoproterenol increased the mass of the left ventricle (+33% ± 4% vs. control; p < 0.05) and right ventricle (+40% ± 9%; p < 0.05). Isoproterenol administration increased the expression of eNOS (+53% ± 12%; p < 0.05) and caveolin-1 (+54% ± 20%, p < 0.05) in the aorta. Relaxation of isolated aorta to acetylcholine and sodium nitroprusside showed a trend towards a worsened endothelial function and a lower sensitivity to exogenous NO. Thus, 1 week of isoproterenol administration led to increased eNOS expression in the aorta without amelioration of endothelial vasorelaxation function. Concomitant increase in caveolin-1 expression may be responsible for this paradox.

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

1996 ◽  
Vol 54 ◽  
pp. 786-787
Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Cardiac Tissues ◽  
Mammalian Tissues ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

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