The vascular endothelium plays an important role in smooth muscle relaxation, vasodilation and eventually regulation of blood flow. Under various pathological conditions (e.g. hyperglycaemia) endothelial cells undergo proinflammatory stimulation that may result in inflammation, severe damage to the vascular endothelium, and eventually blood vessels-related pathology. A critical role in the initiation and acceleration of inflammatory reaction is played by TNF- which belongs to endothelial cell-activating proinflammatory and cytotoxic cytokines. We found that exposition of EA.hy926 cells (endothelial cell line) to 10 nM TNF- for 6 hours stimulates nitric oxide synthesis which is of crucial importance for blood vessel vasodilatation and induces changes in mitochondrial network architecture suggesting cellular stress response. Moreover TNF- enhances mitochondrial biogenesis which is expressed by increased level of transcription factors necessary for mitochondrial protein synthesis and at least some respiratory chain proteins content. This latter effect is similar to that observed in neonatal rat cardiomyocytes treated with bacterial LPS. In conclusion, data presented in this paper indicate that pro-inflammatory stimulation of EA.hy926 endothelial cells with TNF- may induce pro-survival changes in mitochondrial organization and enhance the protein level of respiratory chain complexes which is accompanied by increased oxygen consumption. These observations are in line with those concerning LPS-stimulated muscle cells and suggest a similar mechanism operating in endothelial cells.