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Am J Physiol Lung Cell Mol Physiol 284: L834-L843, 2003. First published January 17, 2003; doi:10.1152/ajplung.00341.2002
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Vol. 284, Issue 5, L834-L843, May 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 Deem2,3, Daniel L. Luchtel4, and Erik R. Swenson2

1 Department of Pediatrics, Children's Hospital and Regional Medical Center, Seattle 98105; and Departments of 2 Medicine, 3 Anesthesiology, and 4 Environmental Health, University of Washington, Seattle, Washington 98108

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.

nitric oxide synthase inhibitors; isolated perfused lung; 1400W; 7-nitroindazole; nitro-L-arginine methyl ester


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