TY - JOUR
T1 - Relationship between changes in brachial artery flow-mediated dilation and basal release of nitric oxide in subjects with Type 2 diabetes
AU - Green, Daniel
AU - Maiorana, A.J.
AU - Tschakovsky, M.E.
AU - Pyke, K.E.
AU - Weisbrod, C.J.
AU - O'Driscoll, G.
PY - 2006
Y1 - 2006
N2 - 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.
AB - 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.
U2 - 10.1152/ajpheart.01176.2005
DO - 10.1152/ajpheart.01176.2005
M3 - Article
C2 - 16565307
SN - 0363-6135
VL - 291
SP - 1193
EP - 1199
JO - American Journal of Physiology: Heart and Circulatory Physiology
JF - American Journal of Physiology: Heart and Circulatory Physiology
IS - 3
ER -