Margus Annuk, Mihkel Zilmer, Bengt Fellström Endothelium-dependent vasodilation and oxidative stress in chronic renal failure: Impact on cardiovascular disease  Margus Annuk, Mihkel Zilmer, Bengt Fellström  Kidney International  Volume 63, Pages S50-S53 (May 2003) DOI: 10.1046/j.1523-1755.63.s84.2.x Copyright © 2003 International Society of Nephrology Terms and Conditions

Figure 1 Reactive oxygen species (ROS) impair vascular function. Vascular function is impaired by injury to endothelial and vascular smooth muscle cell membranes; reaction with nitric oxide (NO) and inactivation; oxidization of tetrahydrobiopterin (BH4) as cofactor of nitric oxide synthase (NOS); peroxidization of low-density lipoprotein (LDL) to oxidized LDL (oxLDL); stimulation of synthesis of asymmetric dimethylarginine (ADMA)-yielding NOS inhibition; inhibition of guanylyl cyclase, which leads to decreased production of cyclic guanosine monophosphate (cGMP), activation of platelet aggregation and adhesion; and oxLDL, formed under influence of ROS, which may cause upregulation of receptors of adhesion molecules on endothelial cells, platelet derived growth factor (PDGF) receptors on smooth muscle cells (SMC), PDGF synthesis by SMC, and HLA expression on monocytes. Abbreviations are: ECM, extracellular matrix; IL-1, interleukin 1; GTP, guanosine triphosphate; mRNA, messenger RNA. Kidney International 2003 63, S50-S53DOI: (10.1046/j.1523-1755.63.s84.2.x) Copyright © 2003 International Society of Nephrology Terms and Conditions