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Am J Physiol Lung Cell Mol Physiol 282: L1057-L1065, 2002. First published November 30, 2001; doi:10.1152/ajplung.00081.2001
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Vol. 282, Issue 5, L1057-L1065, May 2002

Pulmonary vasoconstriction by serotonin is inhibited by S-nitrosoglutathione

Eva Nozik-Grayck, Timothy J. McMahon, Yuh-Chin T. Huang, Christine S. Dieterle, Jonathan S. Stamler, and Claude A. Piantadosi

Departments of Pediatrics and Medicine, Duke University Medical Center, Durham, North Carolina 27710

Nitric oxide (NO) functions as an endothelium-derived relaxing factor by activating guanylate cyclase to increase cGMP levels. However, NO and related species may also regulate vascular tone by cGMP-independent mechanisms. We hypothesized that naturally occurring NO donors could decrease the pulmonary vascular response to serotonin (5-HT) in the intact lung through chemical interactions with 5-HT2 receptors. In isolated rabbit lung preparations and isolated pulmonary artery (PA) rings, 50-250 µM S-nitrosoglutathione (GSNO) inhibited the response to 0.01-10 µM 5-HT. The vasoconstrictor response to 5-HT was mediated by 5-HT2 receptors in the lung, since it could be blocked completely by the selective inhibitor ketanserin (10 µM). GSNO inhibited the response to 5-HT by 77% in intact lung and 82% in PA rings. In PA rings, inhibition by GSNO could be reversed by treatment with the thiol reductant dithiothreitol (10 mM). 3-Morpholinosydnonimine (100-500 µM), which releases NO and O<UP><SUB>2</SUB><SUP>−</SUP></UP> simultaneously, also blocked the response to 5-HT. Its chemical effects, however, were distinct from those of GSNO, because 5-HT-mediated vasoconstriction was not restored in isolated rings by dithiothreitol. In the intact lung, neither NO donor altered the vascular response to endothelin, which activates the same second-messenger vasoconstrictor system as 5-HT. These findings, which did not depend on guanylate cyclase, are consistent with chemical modification by NO of the 5-HT2 G protein-coupled receptor system to inhibit vasoconstriction, possibly by S-nitrosylation of the receptor or a related protein. This study demonstrates that GSNO can regulate vascular tone in the intact lung by a reversible mechanism involving inhibition of the response to 5-HT.

nitric oxide; G protein-coupled receptor


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