Glutathionylation mediates angiotensin II-induced eNOS uncoupling, amplifying NADPH oxidase-dependent endothelial dysfunction.

4 A nonsignificant trend for reduction in O 2 •− by l‐NAME in Ang II‐treated cells in our study ( Figure 2 A and 2 B) may be consistent with a partial reduction in glutathionylated heNOS‐derived O 2 •− , 4 or indicate the coexistence of other uncoupling mechanisms, such as BH4 depletion, that primarily affect the oxidase domain.

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