Nitrite entry into erythrocytes leads to an oxygenation-dependent formation of nitric oxide, because deoxyhaemoglobin reduces nitrite to NO. Escape of some of this NO from the erythrocytes may cause vasodilation and provide a mechanism for matching blood flow with O₂ conditions. The present study evaluated nitrite transport in pig erythrocytes equilibrated to physiological pCO₂ in oxygenated and deoxygenated states. Nitrite was added and nitrite influx and methaemoglobin formation were measured. Nitrite quickly equilibrated across the erythrocyte membrane and then continued to enter as a consequence of its intracellular removal (reactions with haemoglobin). The membrane permeation showed little oxygenation dependency, which contrasts with a preferential permeation of deoxygenated erythrocytes in some fish species. Nitrite transport in pig showed low temperature sensitivity and was not affected by inhibitors of facilitated diffusion (DIDS, phloretin, PCMB). Extracellular pH was stable during nitrite transport. A preferential entry of nitrite at low O₂ saturation would favour deoxyHb-mediated NO formation. However, the reaction in oxygenated erythrocytes could also be important. Nitrite reacts with oxyHb to form non-toxic nitrate and metHb. This provides a detoxification mechanism that can eliminate excess nitrite, while metHb need not rise significantly, because metHb reductase activity regenerates functional Hb. A dynamic balance may accordingly exist between the need for NO release from partly deoxygenated erythrocytes to promote blood flow at low pO₂ and the need for detoxification in oxygenated erythrocytes at inappropriate high nitrite levels. The transport of nitrite into both oxygenated and deoxygenated erythrocyte may support both functions.