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Department of Anesthesiology, University of Virginia Health System, Charlottesville, Virginia 22906
The nitric oxide
(NO)-cGMP signal transduction pathway plays an important role in the
regulation of pulmonary vascular tone and resistance in pulmonary
hypertension. A number of studies have demonstrated that endothelial
(e) and inducible nitric oxide synthases (NOS) are upregulated in
hypoxia-exposed rat lung. These changes in NOS expression have been
found to correlate with the process of pulmonary vascular remodeling in
hypoxia-induced pulmonary hypertension, and remodeling is increased in
the absence of eNOS. In this study, we examined the expression and
localization of soluble guanylate cyclase (sGC), the primary receptor
for NO, in hypoxia- and normoxia-treated rat lungs. Male Sprague-Dawley rats were exposed to hypoxia (10%
O2, normobaric) or normoxia for 1, 3, 5, and 21 days. The lungs were used for Western analysis of sGC
protein, sGC enzyme activity, immunohistochemistry using antiserum
against sGC 
1- and
1-subunits, and nonradioactive in situ hybridization (NRISH) using a digoxigenin-labeled sGC 1-subunit cRNA probe. Western
blot analysis revealed a more than twofold increase of sGC protein
1-subunit in rat lungs exposed to 3, 5, and 21 days of hypoxia, correlating well with sGC enzyme activity. Immunohistochemistry and NRISH demonstrated increased expression of sGC in the smooth muscle cells of the pulmonary arteries
and arterioles in the hypoxic rat lungs when compared with normoxic
controls. Based on our results, the upregulation of sGC may play an
important role in the regulation of smooth muscle tone and pressure in
the pulmonary circulation during chronic hypoxia.
nitric oxide
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