Abstract
Nitric oxide (NO), prostacyclin (PGI2), and thromboxane (TxA2) are produced by NO synthase (NOS) and cyclooxygenase (ie, COX-1 and COX-2) isoforms, respectively. They are highly potent vasoactive molecules. NOS and COX pathways are assumed to interact and modulate each other. Both NOS and COX can produce superoxide which may react with NO to produce peroxynitrite (ONOO−), thus diminishing NO bioactivity. Peroxynitrite may decrease NOS activity, but its action on COX is 2 sided; it may enhance or decrease COX …
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