β-Amyloid induces cerebrovascular endothelial dysfunction in the rat brain

Abstract

β-Amyloid toxicity plays a central role in the pathology of Alzheimer’s disease. Contraction and relaxation responses of pressurized rat posterior cerebral artery were studied before and after in vitro exposure to β-amyloid. The peptide-induced characteristic features of endothelial dysfunction including enhanced vasoconstriction with serotonin and diminished relaxation to endothelium-dependent vasodilators acetylcholine and bradykinin. Response to the endothelium-independent vasodilator nitroprusside was not affected by β-amyloid. β-amyloid inhibition of acetylcholine-induced vasodilation was prevented by the oxygen radical scavenging enzyme superoxide dismutase. Endothelial destruction and the protective effect of superoxide dismutase was verified by electron microscopy. The results suggest that fJ-amyloid peptide produces endothelial dysfunction in cerebral microvessels through reactive oxygen species. [Neural Res 1997; 19: 534-538]