Submitted on November 7, 2005
Accepted on March 17, 2006
RELATIONSHIP BETWEEN CHANGES IN BRACHIAL ARTERY FLOW-MEDIATED DILATION AND BASAL RELEASE OF NITRIC OXIDE IN TYPE II DIABETIC SUBJECTS
Daniel John Green1*, Andrew J. Maiorana2, Michael E. Tschakovsky3, Kyra E Pyke3, Cara J Weisbrod2, and Gerry O'Driscoll2
1 School of Sport and Exercise Science, Liverpool John Moores University, Liverpool, Western Australia, United Kingdom
2 Royal Perth Hospital, Cardiac Transplant Unit, Perth, Western Australia, Australia
3 School of Physical and Health Education, Queens University, Kingston, Canada
* To whom correspondence should be addressed. E-mail: brevis{at}cyllene.uwa.edu.au.
Assessment of flow-mediated dilation (FMD) following forearm ischemia is widely used as a non-invasive 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 randomised cross-over studies was undertaken in 17 subjects with type 2 diabetes; 9 subjects undertook an exercise training or control period, whilst the remaining 8 subjects were administered an angiotensin II receptor blocker or placebo. FMD was assessed using wall-tracking of high-resolution brachial artery ultrasound images in response to reactive hyperemia. Resistance vessel basal endothelium-dependent NO function was assessed using intra-brachial administration of monomethyl arginine (LNMMA) and plethysmographic assessment of forearm blood flow (FBF). FMD was higher following intervention compared to control/placebo (6.15 ± 0.53 vs 3.81 ± 0.72%, P<0.001). There were no significant changes in the FBF responses to LNMMA. Regression analysis between FMD and LNMMA 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 LNMMA 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 Type 2 diabetics.
