Microvascular function in younger adults with obesity and metabolic syndrome: role of oxidative stress.
Older adults with cardiovascular disease exhibit microvascular dysfunction and increased levels of reactive oxygen species (ROS). We hypothesized that microvascular impairments begin early in the disease process and can be improved by scavenging ROS. Forearm blood flow (Doppler ultrasound) was measured in 45 young (32 ± 2 yr old) adults (n = 15/group) classified as lean, obese, and metabolic syndrome (MetSyn). Vasodilation in response to endothelial (ACh) and vascular smooth muscle [nitroprusside (NTP) and epoprostenol (Epo)] agonists was tested before and after intra-arterial infusion of ascorbic acid to scavenge ROS. Vasodilation was assessed as a rise in relative vascular conductance (ml·min(-1)·dl(-1)·100 mmHg(-1)). ACh and NTP responses were preserved (P = 0.825 and P = 0.924, respectively), whereas Epo responses were lower in obese and MetSyn adults (P < 0.05) than in lean controls. Scavenging of ROS via infusion of ascorbic acid resulted in an increase in ACh-mediated (P < 0.001) and NTP-mediated (P < 0.001) relative vascular conductance across all groups, suggesting that oxidative stress influences vascular responsiveness in adults with and without overt cardiovascular disease risk. Ascorbic acid had no effect on Epo-mediated vasodilation (P = 0.267). These results suggest that obese and MetSyn adults exhibit preserved endothelium-dependent vasodilation with reduced dependence on prostacyclin and are consistent with an upregulation of compensatory vascular control mechanisms.
Department of Kinesiology, School of Education, University of Wisconsin, Madison, Wisconsin;
Jacqueline K
JK
Limberg
John W
JW
Harrell
Rebecca E
RE
Johansson
Marlowe W
MW
Eldridge
Lester T
LT
Proctor
Joshua J
JJ
Sebranek
William G
WG
Schrage
D000109:Acetylcholine / Q000494:pharmacology; D000328:Adult; D000975:Antioxidants / Q000494:pharmacology; D001205:Ascorbic Acid / Q000494:pharmacology; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D011464:Epoprostenol / Q000494:pharmacology; D006801:Humans; D007261:Infusions, Intra-Arterial; D024821:Metabolic Syndrome / Q000503:physiopathology*; D055806:Microvessels / Q000187:drug effects / Q000503:physiopathology*; D018482:Muscle, Skeletal / Q000098:blood supply / Q000000981:diagnostic imaging; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000503:physiopathology*; D009599:Nitroprusside / Q000494:pharmacology; D009765:Obesity / Q000503:physiopathology*; D018384:Oxidative Stress; D012039:Regional Blood Flow; D018608:Ultrasonography, Doppler; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology
D000975:Antioxidants; D014665:Vasodilator Agents; D009599:Nitroprusside; D011464:Epoprostenol; D000109:Acetylcholine; D001205:Ascorbic Acid
blood flow; endothelial function; nitric oxide; prediabetes; prostacyclin