Hypercholesterolemia and endothelial dysfunction.
Endothelial cells respond to hemodynamic forces with the expression of different phenotypes with disparate functional properties. At arterial bends and flow dividers, cells are relatively deprived of fluid-shear-stress-induced cell differentiation and exhibit phenotypes with increased mitotic rate, decreased intercellular contact, increased permeability for macromolecules, and the expression of molecules favoring constriction, adhesion, and thrombosis. Arterial sites covered by such cells are vulnerable to the atherogenic effects of hypercholesterolemia. A hallmark of endothelial cells exposed to hypercholesterolemia is a reduced capacity to release endothelium-derived relaxing factor. Pharmacological interventions that suppress or stimulate nitric oxide production appear to enhance or reduce the atherogenic effects of hypercholesterolemia.
Henry
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PD
Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Cabello
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OA
Chen
C H
CH
D000594:Amino Acid Oxidoreductases / Q000378:metabolism; D001120:Arginine / Q000378:metabolism; D001696:Biomechanical Phenomena; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006801:Humans; D006937:Hypercholesterolemia / Q000503:physiopathology*; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase; D014664:Vasodilation
D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase; D000594:Amino Acid Oxidoreductases