Our previous studies demonstrated that vascular wall oxygen consumption rate (QO2) of arteriole under in vivo functional condition was dramatically greater than that reported by isolated vascular segment. Furthermore, such high QO2 of vascular wall decreases during vasodilation. However, it is unknown whether such a reduction in QO2 during vasodilation would be caused by a decrease in consumption of vascular endothelial cell (EC) or smooth muscle. In this study, we aimed to explain whether vascular EC or smooth muscle affects the decrease in vascular wall QO2 during vasodilation. QO2 during EC-dependent and EC-independent vasodilation in rat cremaster muscle was determined using the intra- and peri-vascular PO2 measured by phosphorescence quenching microscopy. EC-dependent vasodilation was induced by increased NO production due to increased blood flow, while EC-independent vasodilation was induced by topical administration of papaverine. EC-dependent and EC-independent vasodilation increased arteriolar diameters by 13% and 17%, respectively, relative to the values under a normal condition. Vascular wall QO2 decreased significantly during both EC-dependent and EC-independent vasodilation as compared with that under a normal condition. Vascular wall QO2 during EC-independent vasodilation was lower than that during EC-dependent vasodilation. However, there was no significant difference between the energy efficiency, which is defined as the variable ratio of circumferential wall tension (amount of mechanical work) to vascular wall QO2 (energy cost) between normal and vasodilated conditions. These results suggest that the decrease in vascular wall QO2 during vasodilation is related to reduced mechanical work of vascular smooth muscle.