Hypochlorous acid impairs endothelium-derived nitric oxide bioactivity through a superoxide-dependent mechanism.

Objective: To determine how hypochlorous acid (HOCl), the principal product of myeloperoxidase, modulates vascular function.

Methods And Results: Rabbit arterial rings exposed to HOCl (0 to 500 micromol/L) exhibited dose- and time-dependent impairment of endothelium-dependent arterial relaxation to acetylcholine and A23187, but not the NO donor, diethylamine NONOate, suggesting that HOCl targets the endothelium. This effect was not because of cytotoxicity, as HOCl treatment produced no significant change in endothelial cell morphology or lactate dehydrogenase release.