Submitted on December 28, 2005
Accepted on February 20, 2006
Vascular wall energetics in arterioles during nitric oxide dependent and independent vasodilation
Masahiro Shibata1*, Kairong Qin2, Shigeru Ichioka1, and Akira Kamiya1
1 Department of Biomedical Engineering, University of Tokyo, Graduate School of Medicine, Tokyo, Japan
2 Department of Biomedical Engineering, University of Tokyo, Graduate School of Medicine, Tokyo, Japan; Institute for Mechanobiology and Medical Engineering, Shanghai Jiao Tong University, Shanghai, China
* To whom correspondence should be addressed. E-mail: shibatam{at}m.u-tokyo.ac.jp.
The objective of this study was to evaluate whether the nitric oxide (NO) released from vascular endothelial cells would decrease vessel wall oxygen consumption by decreasing the energy expenditure of mechanical work by vascular smooth muscle. The oxygen consumption rate 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 laser microscopy. 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 of vessel walls was evaluated by the variable ratio of circumferential wall tension (amount of mechanical work) to vessel wall oxygen consumption rate (energy cost) in the arteriole between normal and vasodilated conditions. NO dependent and independent dilation increased arteriolar diameters by 13% and 17%, respectively, relative to the values under normal condition. Vessel wall oxygen consumption decreased significantly during both NO dependent and independent vasodilation as compared with that under normal condition. However, vessel wall oxygen consumption during NO independent vasodilation was significantly lower than that during NO dependent vasodilation. On the other hand, there was no significant difference between the energy efficiency of vessel walls during NO dependent and independent vasodilation, suggesting the decrease in vessel wall oxygen consumption produced by NO to be related to reduced mechanical work of vascular smooth muscle.
