Dehydroascorbic acid (DHAA) enters cells via Na+-independent glucose transporters (GLUT) and is converted to ascorbate. However, we found that Na+ removal inhibited [14C]DHAA uptake by smooth-muscle cells cultured from pig coronary artery. The uptake was examined for 2–12min at 10–200μM DHAA in either the presence of 134mM Na+ or in its absence (N-methyl d-glucamine, choline or sucrose replaced Na+). This inhibition of DHAA uptake by Na+ removal was paradoxical because it was inhibited by 2-deoxyglucose and cytochalasin B, as expected of transport via the GLUT pathway. We tested the hypothesis that this paradox resulted from an inefficient intracellular reduction of [14C]DHAA into [14C]ascorbate upon intracellular acidosis caused by the Na+ removal. Consistent with this hypothesis: (i) the Na+/H+-exchange inhibitors ethylisopropyl amiloride and cariporide also decreased the uptake, (ii) Na+ removal and Na+/H+-exchange inhibitors lowered cytosolic pH, with the decrease being larger in 12min than in 2min, and (iii) less of the cellular 14C was present as ascorbate (determined by HPLC) in cells in Na+-free buffer than in those in Na+-containing buffer. This inability to obtain ascorbate from extracellular DHAA may be detrimental to the coronary artery under hypoxia-induced acidosis during ischaemia/reperfusion.