P090. Cross talk between endothelial nitric oxide synthase and arginase II

Nitric Oxide ◽  
2006 ◽  
Vol 14 (4) ◽  
pp. 46
Author(s):  
Gokce Topal ◽  
Annie Brunet ◽  
Laurence Walch ◽  
Jean-Luc Boucher ◽  
Monique David-Dufilho
2020 ◽  
Vol 2 (2) ◽  
pp. 1-14
Author(s):  
Prashant Singh ◽  

Background and Purpose Nitrate tolerance can be explained based on the reduction of the vessel responsiveness and the same is used for endogenous vasodilator Nitric Oxide (NO). There are some limitations for the treatment of ischaemia, angina etc. and it attracted the scientists and researchers. The location of arginase II is endothelial cells in mitochondria and it is used to change the potency of endothelial nitric oxide synthase.


Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  

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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