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Departments of 1 Pediatrics, 2 Physiology, and 3 Pathology, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75235
Nitric oxide (NO), generated by NO synthase
(NOS), is an important mediator of physiological processes in the
airway and lung parenchyma, and there is evidence that the pulmonary
expression of the endothelial isoform of NOS (eNOS) is developmentally
regulated. The purpose of the present study was to delineate the
cellular distribution of expression of eNOS in the developing
respiratory epithelium and to compare it with inducible (iNOS) and
neuronal (nNOS) NOS. Immunohistochemistry was performed on fetal
(125-135 days gestation, term 144 days), newborn (2-4 wk),
and maternal sheep lungs. In fetal lung, eNOS expression was evident in
bronchial and proximal bronchiolar epithelia but was absent in terminal and respiratory bronchioles and alveolar epithelium. Similar to eNOS,
iNOS was detected in bronchial and proximal bronchiolar epithelia but
not in alveolar epithelium. However, iNOS was also detected in terminal
and respiratory bronchioles. nNOS was found in epithelium at all levels
including the alveolar wall. iNOS and nNOS were also detected in airway
and vascular smooth muscle. The cellular distribution of all three
isoforms was similar in fetal, newborn, and adult lungs. Findings in
the epithelium were confirmed by isoform-specific reverse
transcription-polymerase chain reaction assays and NADPH diaphorase
histochemistry. Thus the three NOS isoforms are commonly expressed in
proximal lung epithelium and are differentially expressed in distal
lung epithelium. All three isoforms may be important sources of
epithelium-derived NO throughout lung development.
airway; inducible nitric oxide synthase; reduced nicotinamide adenine dinucleotide phosphate diaphorase; neuronal nitric oxide synthase; smooth muscle
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