scholarly journals Environmental exposures, nitric oxide synthase genes, and exhaled nitric oxide in asthmatic children

2009 ◽  
Vol 44 (8) ◽  
pp. 812-819 ◽  
Author(s):  
Adam J. Spanier ◽  
Robert S. Kahn ◽  
Richard W. Hornung ◽  
Ning Wang ◽  
Guangyun Sun ◽  
...  
2019 ◽  
Vol 55 (1) ◽  
pp. 68-75
Author(s):  
Wen‐Xuan Li ◽  
Fei Wang ◽  
Yun‐Qian Zhu ◽  
Li‐Mei Zhang ◽  
Zhen‐Hua Zhang ◽  
...  

2000 ◽  
Vol 162 (4) ◽  
pp. 1262-1267 ◽  
Author(s):  
WOLFGANG STEUDEL ◽  
MAX KIRMSE ◽  
JÖRG WEIMANN ◽  
ROMAN ULLRICH ◽  
JONATHAN HROMI ◽  
...  

Allergy ◽  
2010 ◽  
Vol 66 (3) ◽  
pp. 412-419 ◽  
Author(s):  
M. T. Salam ◽  
T. M. Bastain ◽  
E. B. Rappaport ◽  
T. Islam ◽  
K. Berhane ◽  
...  

2015 ◽  
Vol 49 (19) ◽  
pp. 11859-11865 ◽  
Author(s):  
Renjie Chen ◽  
Liping Qiao ◽  
Huichu Li ◽  
Yan Zhao ◽  
Yunhui Zhang ◽  
...  

2003 ◽  
Vol 284 (5) ◽  
pp. L834-L843 ◽  
Author(s):  
David J. Vaughan ◽  
Thomas V. Brogan ◽  
Mark E. Kerr ◽  
Steven Deem ◽  
Daniel L. Luchtel ◽  
...  

We investigated the source(s) for exhaled nitric oxide (NO) in isolated, perfused rabbits lungs by using isozyme-specific nitric oxide synthase (NOS) inhibitors and antibodies. Each inhibitor was studied under normoxia and hypoxia. Only nitro-l-arginine methyl ester (l-NAME, a nonselective NOS inhibitor) reduced exhaled NO and increased hypoxic pulmonary vasoconstriction (HPV), in contrast to 1400W, an inhibitor of inducible NOS (iNOS), and 7-nitroindazole, an inhibitor of neuronal NOS (nNOS). Acetylcholine-mediated stimulation of vascular endothelial NOS (eNOS) increased exhaled NO and could only be inhibited by l-NAME. Selective inhibition of airway and alveolar epithelial NO production by nebulized l-NAME decreased exhaled NO and increased hypoxic pulmonary artery pressure. Immunohistochemistry demonstrated extensive staining for eNOS in the epithelia, vasculature, and lymphatic tissue. There was no staining for iNOS but moderate staining for nNOS in the ciliated cells of the epithelia, lymphoid tissue, and cartilage cells. Our findings show virtually all exhaled NO in the rabbit lung is produced by eNOS, which is present throughout the airways, alveoli, and vessels. Both vascular and epithelial-derived NO modulate HPV.


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