Ischemia-reperfusion selectively impairs nitric oxide-mediated dilation in coronary arterioles: counteracting role of arginase.

@article{Hein2003IschemiareperfusionSI,
  title={Ischemia-reperfusion selectively impairs nitric oxide-mediated dilation in coronary arterioles: counteracting role of arginase.},
  author={Travis W. Hein and Cuihua Zhang and Wei Wang and C I Chang and Naris Thengchaisri and Lih Kuo},
  journal={FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
  year={2003},
  volume={17 15},
  pages={2328-30}
}
A reduction in L-arginine availability has been implicated in the impairment of endothelium-dependent nitric oxide (NO)-mediated vasodilation by ischemia-reperfusion (I/R). However, the mechanisms contributing to dysregulation of the L-arginine pool remain unknown. Because endothelial cells can metabolize L-arginine via two major enzymes, that is, NO synthase (NOS) and arginase, we hypothesized that up-regulation of arginase during I/R reduces L-arginine availability to NOS and thus impairs NO… CONTINUE READING

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