TY - JOUR
T1 - Sympathetic activation markedly reduces endothelium-dependent, flow-mediated vasodilation
AU - Hijmering, Michel L.
AU - Stroes, Erik S. G.
AU - Olijhoek, Jobien
AU - Hutten, Barbara A.
AU - Blankestijn, Peter J.
AU - Rabelink, Ton J.
PY - 2002
Y1 - 2002
N2 - OBJECTIVES We sought to evaluate whether increased sympathetic outflow may interfere with flow-mediated dilation (FMD). BACKGROUND Endothelial function, assessed as FMD, is frequently used as an intermediate end point in intervention studies. Many disease states with increased sympathetic tone are also characterized by endothelial dysfunction. METHODS Sixteen healthy volunteers underwent FMD studies with and without concomitant sympathetic stimulation. Intra-arterial nitroglycerin (NTG) infusion was used to assess endothelium-independent vasodilation. Pathophysiologically relevant sympathetic stimulation was achieved by baroreceptor unloading, using a lower body negative pressure box. In a subset of eight volunteers, this protocol was repeated during loco-regional alpha-adrenergic blockade by intra-arterial infusion of phentolamine (PE). Reactive hyperemic flow was assessed with strain-gauge phlethysmography. RESULTS Overall, FMD responses (8.3 +/- 3.4%) were significantly attenuated by concomitant sympathetic stimulation (3.6 +/- 3.4%, p <0.01). Loco-regional alpha-adrenergic blockade had no effect on baseline FMD responses (10.7 +/- 4.7%), whereas the attenuation by sympathetic stimulation was abolished completely during PE co-infusion (11.5 +/- 3.3%). During intra-arterial NTG infusions, arterial diameters relative to baseline were not significantly different between the four possible stages. CONCLUSIONS Sympathetic stimulation, at a clinically relevant range, significantly impairs the FMD response by an alpha-adrenergic mechanism. (C) 2002 by the American College of Cardiology
AB - OBJECTIVES We sought to evaluate whether increased sympathetic outflow may interfere with flow-mediated dilation (FMD). BACKGROUND Endothelial function, assessed as FMD, is frequently used as an intermediate end point in intervention studies. Many disease states with increased sympathetic tone are also characterized by endothelial dysfunction. METHODS Sixteen healthy volunteers underwent FMD studies with and without concomitant sympathetic stimulation. Intra-arterial nitroglycerin (NTG) infusion was used to assess endothelium-independent vasodilation. Pathophysiologically relevant sympathetic stimulation was achieved by baroreceptor unloading, using a lower body negative pressure box. In a subset of eight volunteers, this protocol was repeated during loco-regional alpha-adrenergic blockade by intra-arterial infusion of phentolamine (PE). Reactive hyperemic flow was assessed with strain-gauge phlethysmography. RESULTS Overall, FMD responses (8.3 +/- 3.4%) were significantly attenuated by concomitant sympathetic stimulation (3.6 +/- 3.4%, p <0.01). Loco-regional alpha-adrenergic blockade had no effect on baseline FMD responses (10.7 +/- 4.7%), whereas the attenuation by sympathetic stimulation was abolished completely during PE co-infusion (11.5 +/- 3.3%). During intra-arterial NTG infusions, arterial diameters relative to baseline were not significantly different between the four possible stages. CONCLUSIONS Sympathetic stimulation, at a clinically relevant range, significantly impairs the FMD response by an alpha-adrenergic mechanism. (C) 2002 by the American College of Cardiology
U2 - https://doi.org/10.1016/S0735-1097(01)01786-7
DO - https://doi.org/10.1016/S0735-1097(01)01786-7
M3 - Article
C2 - 11849869
SN - 0735-1097
VL - 39
SP - 683
EP - 688
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 4
ER -