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J Am Coll Cardiol, 1999; 34:631-638
© 1999 by the American College of Cardiology Foundation
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Assessment and treatment of endothelial dysfunction in humans

Todd J. Anderson, MD, FRCPCa,1

a Cardiology Division, Department of Medicine, University of Calgary, Calgary, Alberta, Canada



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Figure 1 High-resolution ultrasound image of brachial artery at baseline and 1 min after upper-arm occlusion cuff release and subsequent flow-mediated vasodilation.

 


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Figure 2 Oxidative stress leads to attenuation of endothelium-dependent vasodilation by: 1) decreased production of NO through oxidized LDL-mediated mechanisms, and by 2) increased destruction of NO by superoxide. See text for details. Gi = pertussis sensitive G protein; O2 = superoxide anion; ONOO = peroxynitrite anion; PKC = protein kinase C; cNOS = constitutive form of nitric oxide synthase; ET = endothelin; AT II = angiotensin II; ox-LDL = oxidized LDL; lyso PC = lysophosphatidylcholine; sGC = soluble guanylate cyclase; cGMP = cyclic guanosine monophosphate; NFKB = nuclear factor kappa beta.

 





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