Endothelium-derived nitric oxide (NO) in addition to its antiplatelet and vasodilatory properties, inhibits proliferation and migration of vascular smooth muscle cells (VSMC), what is the basic event in arterial wall remodeling, restenosis, or atherosclerotic plaque formation. Since reendothelisation may be the limiting step for the formation of neointima, the induction of the angiogenic, endothelial growth factor (VEGF), and iNOS genes expression were investigated using RT-PCR at different time periods (0-48 hrs, 7 and 14 days) of the experimental model of the baloon-induced injury of rabbit carotid artery, as well as in the IL-1β (10ng/ml) - activated VSMC in culture. Influence of the human native or ox-LDL (10-100μg/ml) (modified by 15 hour - lasting incubation with 5μM Cu at 37°C) on the IL-1β- induced iNOS and VEGF gene expression in VSMC was also studied. The influence of VEGF(3-30ng/ml) on NO generation by HUVEC was measured using the NO-selective electrode in the presence of SOD (100U/ml). Baloon-induced denudation resulted in the iNOS expression in the damaged, but not in the sham -operated arteries, observed during the first 24 hours starting from 3 hours after injury, but was not detected after 48 hrs or two weeks later. Expression of the latent isoform VEGF 1 2 0 / 1 2 1 was found in the control arteries, when the expression of the active VEGF 1 6 4 / 1 6 5 isoform was observed starting 6 hours after surgery. IL-1β causes induction of iNOS (after 2-3 hrs) and VEGF 1 6 4 / 1 6 5 (after 6 hours), thus expression of iNOS exceeded the induction of VEGF by 3 hours. Native and modified LDL itself did not induce the measured gene induction, however ox -LDL, but not native LDL inhibited the expression of iNOS as well as VEGF in IL-1β activated cells. Similarily, exogenous NO (DETA/NO) inhibited the IL-1β-induced expression of VEGF. Exogenous VEGF 1 6 5 incubated with HUVEC was able to activate the immediate NO release. We conclude that baloon injury after PTCA cause the induction of VEGF, which promote the reendothelisation of vessel wall. The NO generated by newly formed endothelium may be the limiting step for the excess of expression of the angiogenic VEGF.