The objective of this study was to evaluate whether the nitric oxide (NO) would decrease vessel wall oxygen consumption by decreasing the mechanical work of vascular smooth muscle. The oxygen consumption rate (QO2) of arteriolar walls in rat cremaster muscle was determined in vivo during NO dependent and -independent vasodilation based on the intra- and perivascular oxygen tension (PO2) measured by phosphorescence quenching technique. NO dependent vasodilation was induced by increased NO production due to increased blood flow, while NO independent vasodilation was induced by topical administration of papaverine. The energy efficiency was evaluated by the variable ratio of wall tension to QO2 between normal and vasodilated conditions. NO dependent and -independent dilation increased arteriolar diameters by 13% and 17%, respectively. Vascular wall QO2 decreased significantly during both dilations. There was no significant difference between the energy efficiency during NO dependent and -independent vasodilation, suggesting the decrease in vascular wall QO2 produced by NO to be related to a decrease in the mechanical work of vascular smooth muscle.