Hypothetical scheme illustrating the possible mechanisms that lead to endothelial nitric oxide synthase (eNOS) uncoupling (thick lines/arrows), which results in a reduction of nitric oxide (NO) release and an exacerbation of superoxide anion (•O2-) production, generating peroxynitrite (•ONOO-) and thus, leading to impaired vasodilation. The main causes of the generation of excessive •O2- and the resultant endothelial dysfunction are highlighted. Abbreviations (some are listed in Figure 3): ADMA, asymmetric dimethyl-L-arginine; Ang II, angiotensin II; AT1R, Ang II type 1 receptor; CRP, C-reactive protein; Lox, lipoxygenases; oxLDL, oxidized low-density lipoprotein.
Meyrelles et al. Lipids in Health and Disease 2011 10:211 doi:10.1186/1476-511X-10-211