This brief overview discusses the ability of mediators associated with vascular injury, such as interleukin-1 beta and tumour necrosis factor alpha, to activate vascular smooth muscle cells to produce nitric oxide or a related donor of nitric oxide. The cytokines cause the synthesis of nitric oxide synthase(s), which catalyzes the conversion of L-arginine to nitric oxide and L-citrulline. The production of nitric oxide can be modulated by factors produced by vascular cells and formed elements of the blood (e.g. platelet-derived growth factor, transforming growth factor beta), but also by those generated at sites of vascular injury from inactive precursors circulating in the blood (e.g. thrombin, plasmin). The production of nitric oxide by vascular smooth muscle cells may contribute to the homeostasis of blood vessels at sites of injury. In particular, nitric oxide may prevent the local development of vasospasms, unwanted proliferation of smooth muscle cells, and also help to control coagulation and the formation of the thrombus.