KO-mice for bFGF show reduced systemic blood pressure. The reason for that is not completely understood so far. We hypothesized that nitric oxide (NO) play a critical role by interacting with growth factors and investigated NO effects on bFGF and VEGF, both involved in vascular remodeling. Endothelial cells (HUVEC) were used throughout the study. Only VEGF (10ng/ml) or histamine (1mg/ml), used as independent control, induced NO production (NO2) (3-fold after 6h, n=8, p<0.05), whereas bFGF (3ng/ml) even inhibited NO production if combined with VEGF or histamine. These effects were abolished by bFGF receptor antagonist or wortmannin, indicating a PI3 Kinase dependent signaling. Likewise, in shear stress experiments (16dyn/cm²) bFGF receptor blockers led to a higher NO formation as control shear exposure did. Inhibition by bFGF and induction by VEGF on NO production were reversely reflected by their interplay with NO. Exogenous NO (SNAP, 1mM) inhibited only bFGF-induced migration (50%, n=4x10, p<0.05). bFGF induced capillary-like-structure formation was, however, increased 2-fold if basal NO production was inhibited (LNA, 30mM) whereas VEGF-induced sprouting was reduced. NO modulates vascular remodeling and angiogenesis by opposed effects on VEGF and bFGF. Moreover, bFGF might limit flow-induced NO production and prevents an overshooting in dilatation and by that participate in local blood pressure regulation.