Due to its unique position in the vessel wall, the endothelium acts as a barrier and thereby controls adhesion, aggregation and invasion of immune competent cells. Apoptosis of endothelial cells may critically disturb the integrity of the endothelial monolayer and contribute to the initiation of proinflammatory events. Endothelial cell apoptosis is counteracted by nitric oxide synthesised by the endothelium nitric oxide synthase (eNOS). Thus, nitric oxide inhibits endothelial cell apoptosis induced by proinflammatory cytokines and proatherosclerotic factors including reactive oxygen species and angiotensin II. The apoptosis-suppression may contribute to the profound anti-inflammatory and anti-atherosclerotic effects of endothelial-derived NO. Furthermore, the support of endothelial cell survival by NO may further play a central role for the pro-angiogenic effects of NO.