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• W2093107728 startingPage "1044" @default.
• W2093107728 abstract "Reduced nitric oxide (NO) bioavailability and impaired vascular function are the key pathological characteristics of inflammatory diseases such as atherosclerosis. We have recently found that leukocyte-derived hypochlorous acid is able to react with the nitric-oxide synthase (NOS) substrate l-arginine to produce chlorinated l-arginine (cl-l-Arg). Interestingly, cl-l-Arg potently inhibits the formation of NO metabolites in cultured endothelial cells. It is unknown whether cl-l-Arg has a direct inhibitory effect on endothelial NOS <b>(</b>eNOS). In addition, the effect of cl-l-Arg on the other NOS isoforms, neuronal NOS (nNOS) and inducible NOS (iNOS), is also unknown. Therefore, we designed the current study to test the effects of cl-l-Arg on eNOS, nNOS, and iNOS. Using recombinant NOS, we found that cl-l-Arg had a direct inhibitory effect on the activity of NOS. The effect of cl-l-Arg on NOS activity is nonselective, as all three NOS isoforms were inhibited with a similar IC₅₀. We further determined the effect of cl-l-Arg on the three NOS isoforms at the tissue level. The results demonstrated that cl-l-Arg potently inhibited all three NOS isoform-mediated vessel reactivities, as well as the NOS signaling molecule cGMP. Cl-l-Arg might serve as a novel endogenous NOS inhibitor and an important mediator for vascular dysfunction under inflammatory conditions such as atherosclerosis. Blocking cl-l-Arg formation may be a new therapeutic approach to cardiovascular diseases." @default.
• W2093107728 created "2016-06-24" @default.
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• W2093107728 date "2006-05-22" @default.
• W2093107728 modified "2023-09-27" @default.
• W2093107728 title "l-Arginine Chlorination Results in the Formation of a Nonselective Nitric-Oxide Synthase Inhibitor" @default.
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• W2093107728 doi "https://doi.org/10.1124/jpet.106.104422" @default.
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