Figure 2
From: Mechanisms of endothelial dysfunction in rheumatoid arthritis: lessons from animal studies
Schematic representation of the mechanisms involved in decreased nitric oxide (NO) production in endothelial cells from arthritic rats. Endothelial nitric oxide synthase (eNOS) catalyses the conversion of L-arginine to NO. The upregulation of arginase pathway and the deficit in the co-factor of eNOS tetrahydrobiopterin (BH4) cause uncoupling of eNOS to generate superoxide anions (O2–) which subsequently scavenge NO to generate peroxynitrite (ONOO−). Angiotensin-II (ANG-II) might amplify O2– production by activating NADPH (reduced form of nicotinamide adenine dinucleotide phosphate) oxidase after ANG-II type 1 (AT1) receptor activation. Up and down arrows indicate increases or decreases in amount or activity (from [14–23]).