Key result
S-nitrosylation of soluble guanylyl cyclase results in decreased responsiveness to NO, which can be prevented by increasing cellular thiols or mutating specific cysteines.
Population
Primary aortic smooth muscle cells, human umbilical vein endothelial cells, isolated aorta, and semipurified…
Design
Preclinical
Authors
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S-nitrosylation may underlie NO tolerance in smooth muscle; animal data leaves open whether thiol augmentation or cysteine targeting mitigates clinical resistance.
S-nitrosylation of sGC directly causes its desensitization to NO, revealing a molecular mechanism that could explain NO tolerance in smooth muscle cells.
Sayed et al. (2007) studied this question. S-nitrosylation (via S-nitrosocysteine) was evaluated on sGC responsiveness to NO. S-nitrosylation of soluble guanylyl cyclase results in decreased responsiveness to NO, which can be prevented by increasing cellular thiols or mutating specific cysteines.
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