Acute myocardial infarction remains a major cause of morbidity and mortality worldwide. As such, there is a need for improved cardioprotective strategies. Nitrite represents an alternative source of bioactive nitric oxide (NO) particularly during hypoxia , and recent studies have demonstrated that nitrite is protective against myocardial ischemia reperfusion (I/R) injury . Several mechanisms of nitrite bioconversion to NO have been proposed, such as xanthine oxidase , deoxyhaemoglobin and myoglobin , but the cytoprotective effects of nitrite therapy remains to be elucidated. Recent experimental data have shown that mice deficient in endothelial nitric oxide synthase (eNOS) exhibit reduced steady state levels of both plasma and cardiac nitrite levels when compared to the wild-type mice. Thus suggesting that nitrite restores NO bioavailability . Herein, we have investigated whether these effects are translated in man and therefore assessed the effects of nitrite therapy on eNOS phosphorylation and expression in human left ventricle (LV) biopsies.