Nitric oxide (NO) is intimately involved in vascular homeostasis through its antiplatelet,
antiproliferative, and vasodilating actions. Because of these beneficial properties, methods
of harnessing NO for the prevention of vascular injury responses, such as intimal
hyperplasia, are being explored. One such method involves gene transfer of an NO
synthase (NOS) to sites of vascular injury to provide for local NO synthesis. Gene delivery of
the inducible NOS (iNOS) cDNA to sites of vascular injury in animal models dramatically …