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- W2314839957 abstract "Amyloid beta-peptide (A beta) deposition has been associated with coronary heart disease and neurodegenerative diseases. A link between A beta and free radical generation has been explored in neuronal tissue. We report here on the effect of A beta on pressurized segments of coronary resistance arteries and the role of free radicals. A small oscillatory response to A beta (10[-6] M) that consisted of a relaxation followed by constriction and a return to the basal diameter was observed in all vessels. The thromboxane A2 analog U46619 produced a significantly greater constriction compared with the response before treatment with A beta. The presence of the antioxidant enzyme superoxide dismutase (SOD) reduced both the response to A beta alone and the enhanced response to U46619. Vasodilation responses to acetylcholine (10[-9]-10[-5] M) were virtually eliminated at all concentrations by A beta. We confirmed endothelial cell damage by A beta with electron microscopy. The results suggest that A beta deposition in coronary resistance arteries causes endothelial damage that is mediated through superoxide radicals." @default.
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- W2314839957 date "1997-10-01" @default.
- W2314839957 modified "2023-09-26" @default.
- W2314839957 title "β-Amyloid-Induced Coronary Artery Vasoactivity and Endothelial Damage" @default.
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- W2314839957 doi "https://doi.org/10.1097/00005344-199710000-00017" @default.
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