| Literature DB >> 9883742 |
E S Stroes1, E E van Faassen, G J van Londen, T J Rabelink.
Abstract
Impaired nitric oxide (NO) activity in proatherosclerotic states has been suggested to be caused mainly by increased degradation of NO by oxygen radicals. In recent years, endothelial NO synthase has been identified as a system that contributes to oxygen radical stress under pathophysiologic conditions. We discuss the origin of NO synthase-derived superoxide production, as well as possibilities to modulate (pathologic) shifts in NO/superoxide production by endothelial NO synthase.Entities:
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Year: 1998 PMID： 9883742
Source DB: PubMed Journal: J Cardiovasc Pharmacol ISSN： 0160-2446 Impact factor: 3.105