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Am J Physiol Lung Cell Mol Physiol (January 17, 2003). doi:10.1152/ajplung.00341.2002
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Submitted on October 15, 2002
Accepted on January 14, 2003

Contributions of Nitric Oxide Synthase Isozymes to Exhaled Nitric Oxide and Hypoxic Pulmonary Vasoconstriction in Rabbit Lungs

David J. Vaughan1, Thomas V. Brogan1, Mark E. Kerr2, Steven Deem3, Daniel L. Luchtel4, and Erik R. Swenson2*

1 Department of Pediatrics, Childrens Hospital and Regional Medical Center, Seattle, WA, USA
2 Department of Medicine, University of Washington, Seattle, WA, USA
3 Department of Anesthesiology, University of Washington, Seattle, WA, USA; Department of Medicine, University of Washington, Seattle, WA, USA
4 Department of Environmental Health, University of Washington, Seattle, WA, USA

* To whom correspondence should be addressed. E-mail: eswenson{at}u.washington.edu.

We investigated the source(s) for exhaled 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 L-NAME (a non-selective 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 PAP. 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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