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This Article Full Text Full Text (PDF) All Versions of this Article: 291/3/H1193    most recent 01176.2005v1 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 PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Green, D. J. Articles by O’Driscoll, G. Search for Related Content PubMed PubMed Citation Articles by Green, D. J. Articles by O’Driscoll, G.

Relationship between changes in brachial artery flow-mediated dilation and basal release of nitric oxide in subjects with Type 2 diabetes

¹School of Sport and Exercise Science, Liverpool John Moores University, Liverpool, United Kingdom; ²School of Human Movement and Exercise Science, The University of Western Australia, Nedlands, Australia; ³School of Physical and Health Education, Queens University, Kingston, Ontario, Canada; ⁴Cardiac Transplant Unit, Royal Perth Hospital, Perth, Australia; and ⁵College of Medicine, University of Notre Dame, Fremantle, Australia

Submitted 7 November 2005 ; accepted in final form 17 March 2006

Assessment of flow-mediated dilation (FMD) after forearm ischemia is widely used as a noninvasive bioassay of stimulated nitric oxide (NO)-mediated conduit artery vasodilator function in vivo. Whether this stimulated endothelial NO function reflects basal endothelial NO function is unknown. To test this hypothesis, retrospective analysis of randomized crossover studies was undertaken in 17 subjects with Type 2 diabetes; 9 subjects undertook an exercise training or control period, whereas the remaining 8 subjects were administered an angiotensin II receptor blocker or placebo. FMD was assessed by using wall tracking of high-resolution brachial artery ultrasound images in response to reactive hyperemia. Resistance vessel basal endothelium-dependent NO function was assessed by using intrabrachial administration of N^G-monomethyl-L-arginine (L-NMMA) and plethysmographic assessment of forearm blood flow (FBF). FMD was higher after intervention compared with control/placebo (6.15 ± 0.53 vs. 3.81 ± 0.72%, P < 0.001). There were no significant changes in the FBF responses to L-NMMA. Regression analysis between FMD and L-NMMA responses at entry to the study revealed an insignificant correlation (r = –0.10, P = 0.7), and improvements in FMD with the interventions were not associated with changes in the L-NMMA responses (r = –0.04, P = 0.9). We conclude that conduit artery-stimulated endothelial NO function (FMD) does not reflect basal resistance vessel endothelial NO function in subjects with Type 2 diabetes.

exercise; acetylcholine; resistance vessel; conduit artery