Nitric oxide (NO) and related reactive nitrogen species have several effects on mitochondria that may impact cell death and survival of cells in cardiovascular system. NO can cause rapid but reversible inhibition of mitochondrial respiration which may synergize with hypoxia to induce cell death. NO and reactive nitrogen species may cause production of reactive oxygen species which may have signalling role in the cells or may induce cell death. Reactive nitrogen species also activate mitochondrial permeability transition pore leading to apoptotic or necrotic cell death. Recently we and others have found that low concentrations of NO may activate signalling pathways involving activation of protein kinase G and leading to increased resistance of mitochondria to opening of permeability transition pore. This may have important cardioprotective effect in heart ischaemia/reperfusion. The mechanism of such protective effect will be discussed.