HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 289/6/H2673    most recent 00420.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Shibata, M. Articles by Kamiya, A. Search for Related Content PubMed PubMed Citation Articles by Shibata, M. Articles by Kamiya, A.

Nitric oxide modulates oxygen consumption by arteriolar walls in rat skeletal muscle

Department of Biomedical Engineering, Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo, Japan

Submitted 28 April 2005 ; accepted in final form 15 July 2005

To study the role of nitric oxide (NO) in regulating oxygen consumption by vessel walls, the oxygen consumption rate of arteriolar walls in rat cremaster muscle was measured in vivo during flow-induced vasodilation and after inhibiting NO synthesis. The oxygen consumption rate of arteriolar walls was calculated based on the intra- and perivascular PO₂ values measured by phosphorescence quenching laser microscopy. The perivascular PO₂ value of the arterioles during vasodilation was significantly higher than under control conditions, although the intravascular PO₂ values under both conditions were approximately the same. Inhibition of NO synthesis, on the other hand, caused a significant increase in arterial blood pressure and a significant decrease in arteriolar diameter. Inhibition of NO synthesis also caused a significant decrease in both the intra- and perivascular PO₂ values of the arterioles. Inhibition of NO synthesis increased the oxygen consumption rate of the vessel walls by 42%, whereas enhancement of flow-induced NO release decreased it by 34%. These results suggest that NO plays an important role not only as a regulator of peripheral vascular tone but also as a modulator of tissue oxygenation by reducing oxygen consumption by vessel walls. In addition, enhancement of NO release during exercise may facilitate efficient oxygen supply to the surrounding high metabolic tissue.

flow-induced vasodilation; N-nitro-L-arginine methyl ester; oxygen transport; vascular tone; vascular endothelial cells

This article has been cited by other articles:

				C.-L. Leong, W. P. Anderson, P. M. O'Connor, and R. G. Evans Evidence that renal arterial-venous oxygen shunting contributes to dynamic regulation of renal oxygenation Am J Physiol Renal Physiol, June 1, 2007; 292(6): F1726 - F1733. [Abstract] [Full Text] [PDF]

				M. Shibata, K. Qin, S. Ichioka, and A. Kamiya Vascular wall energetics in arterioles during nitric oxide-dependent and -independent vasodilation J Appl Physiol, June 1, 2006; 100(6): 1793 - 1798. [Abstract] [Full Text] [PDF]

				P. Cabrales, A. G. Tsai, and M. Intaglietta Nitric oxide regulation of microvascular oxygen exchange during hypoxia and hyperoxia J Appl Physiol, April 1, 2006; 100(4): 1181 - 1187. [Abstract] [Full Text] [PDF]