Effects of Chronic Hypoxia and Altered Hemodynamics on Endothelial Nitric Oxide Synthase and Preproendothelin-1 Expression in the Adult Rat Lung

CHEST Journal ◽  
1998 ◽  
Vol 114 (1) ◽  
pp. 35S-36S ◽  
Author(s):  
Timothy D. Le Cras ◽  
Robert C. Tyler ◽  
Marilee P. Horan ◽  
Ken G. Morris ◽  
Ivan F. McMurty ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Chronic Hypoxia ◽  
Rat Lung ◽  
Adult Rat ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

scholarly journals Effects of chronic hypoxia and altered hemodynamics on endothelial nitric oxide synthase expression in the adult rat lung.

1998 ◽  
Vol 101 (4) ◽  
pp. 795-801 ◽  
Author(s):  
T D Le Cras ◽  
R C Tyler ◽  
M P Horan ◽  
K G Morris ◽  
R M Tuder ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Chronic Hypoxia ◽  
Rat Lung ◽  
Adult Rat ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

scholarly journals Chronic hypoxia induces right heart failure in caveolin-1−/− mice

2012 ◽  
Vol 302 (12) ◽  
pp. H2518-H2527 ◽  
Author(s):  
J. Agustin Cruz ◽  
Eileen M. Bauer ◽  
Andres I. Rodriguez ◽  
Archana Gangopadhyay ◽  
Nabil S. Zeineh ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Chronic Hypoxia ◽  
Left Ventricular ◽  
Caveolin 1 ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Rv Function

Caveolin-1 (Cav-1)−/− mice develop mild pulmonary hypertension as they age. In this study, we sought to determine the effect of chronic hypoxia, an established model of pulmonary hypertension, on young Cav-1−/− mice with no measurable signs of pulmonary hypertension. Exposure of Cav-1−/− mice to chronic hypoxia resulted in an initial rise in right ventricular (RV) systolic pressure (RVSP) similar to wild-type (WT) mice. By three weeks RVSP decreased in the Cav-1−/− mice, whereas it was maintained in WT mice. The drop in RVSP in Cav-1−/− mice was accompanied by decreased cardiac output, increased RV hypertrophy, RV interstitial fibrosis, decreased RV sarco(endo)plasmic reticulum Ca2+-ATPase 2a mRNA and decreased RV function compared with WT mice. Importantly, minimal differences were noted in pulmonary vascular remodeling between WT and Cav-1−/− mice, and left ventricular function was normal in hypoxic Cav-1−/− mice. Mechanistically, increased endothelial nitric oxide synthase uncoupling and increased tyrosine nitration of protein kinase G were detected in the RV of Cav-1−/− mice. These hemodynamic, histological, and molecular changes were prevented in Cav-1−/− mice expressing an endothelial-specific Cav-1 transgene or by nitric oxide synthase inhibition. These data suggest that, in Cav-1−/− mice, increased oxidative/nitrosative stress due to endothelial nitric oxide synthase uncoupling modifies the response of the RV to pressure overload, accelerating the deterioration of RV function.

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).

Sign in / Sign up

Export Citation Format

Share Document