Nitrite has long been considered an inert oxidative metabolite of nitric oxide (NO). However, recent experimental findings strongly suggest that nitrite is a critical storage form of NO that is converted back into NO during ischemic or hypoxic events as well as under physiological conditions. Thus, the conversion of nitrite into NO during cellular stress may be an evolutionarily conserved and redundant means for NO generation at a time when endothelial nitric oxide synthase is non-functional. As a result of the recent revelation that the nitrite anion serves an important biological function a large number of studies have been performed to characterize both the physiological actions and therapeutic potential of nitrite under diverse conditions. While the earliest experiments characterized the vasodilatory effects of nitrite in both animal models and humans, more recent research efforts have focused on the potential benefits of nitrite in a number of pathological states. Nitrite therapy has now been studied in numerous animal models and has proven to be an effective means to ameliorate myocardial ischemia-reperfusion (I/R) injury. This review will focus on recent experimental findings related to the cytoprotective actions of nitrite therapy in the setting of myocardial I/ R injury.