BACKGROUND: Endothelial derived nitric oxide (NO) is essential in the regulation of blood pressure and attenuates leukocyte-endothelial interactions associated with vascular injury. Endothelial NO synthase (eNOS) is coupled to L-arginine in the presence of tetrahydrobiopetrin (BH4) to produce NO. However, when BH4 is oxidized to dihydrobiopetrin (BH2) under conditions of oxidative stress, the ratio of BH2 to BH4 is increased causing the uncoupling of eNOS to use molecular oxygen as a substrate, instead of L-arginine, to produce superoxide
