Inducible NO synthase dependent S-nitrosylation and activation of arginase1 contribute to age-related endothelial dysfunction.

@article{Santhanam2007InducibleNS,
  title={Inducible NO synthase dependent S-nitrosylation and activation of arginase1 contribute to age-related endothelial dysfunction.},
  author={Lakshmi Santhanam and Hyun Kyo Lim and Hyun Kyoung Lim and Victor A Miriel and Tashalee R. Brown and Meet S Patel and Sarit Ella Balanson and Sungwoo Ryoo and Mirinda Anderson and Kaikobad Irani and Firdous Ahmad Khanday and Luigi Di Costanzo and Daniel P Nyhan and Joshua M Hare and David W Christianson and Richard J Rivers and Artin A. Shoukas and Dan E. Berkowitz},
  journal={Circulation research},
  year={2007},
  volume={101 7},
  pages={692-702}
}
Endothelial function is impaired in aging because of a decrease in NO bioavailability. This may be, in part, attributable to increased arginase activity, which reciprocally regulates NO synthase (NOS) by competing for the common substrate, L-arginine. However, the high Km of arginase (>1 mmol/L) compared with NOS (2 to 20 micromol/L) seemingly makes direct competition for substrate unlikely. One of the mechanisms by which NO exerts its effects is by posttranslational modification through S… CONTINUE READING