The formation of stable NO donors from reactions of ONOO- with glycerol, glucose, or thiols is not species specific, sine these compounds are physiologically active in arteries of different species. These NO donors produce a slowly developing and sustained decrease in tension consistent with the time required for the metabolic conversion of the NO donor to an NO- releasing metabolite. In vitro, NO donors are formed from the reaction of ONOO- with plasma and induce vascular relaxation and inhibit platelet aggregation, through a mechanism that is inhibited by the NO scavenger oxyHb. The pathophysiological consequences of the reactions of ONOO- with polyhydroxylated compounds are currently being investigated. Potential pathways involved in the formation of NO donors by ONOO- under pathological conditions are summarized in Fig. 4. In vivo, NO-dependent nitration and nitrosation reactions may be enhanced at sites of inflammation. Current thinking suggests that the increased production of O2-, in inflammatory cells, facilitates ONOO- formation and thus leads to the modification of NO reactivity in the blood vessel wall.
