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Abstract
We characterized the acute effects of oxidized low-density lipoproteins (oxidized-LDL)
on vascular reactivity in isolated aorta from wild-type C57BL/6J mice, and compared
these with the chronic alterations in vascular function observed in apolipoprotein-E
gene knockout [ApoE(-/-)] mice fed a high-fat diet, which results in hyperlipidemia
and atherosclerosis. In the abdominal (but not thoracic) aorta, oxidized-LDL (100
microg/ml) reduced relaxations induced by acetylcholine (10(-9) M-10(-5) M), which
are mediated entirely by nitric oxide (NO). The relaxations induced by the NO donor
S-nitroso-N-acetylpenicillamine (SNAP, 10(-8) M-10(-4) M), the cyclic GMP analogue
8-bromo cyclic GMP (100 microM) and the nonspecific vasodilator papaverine (100 microM)
were not changed by oxidized-LDL. Native LDL had no effect on vasorelaxations. The
attenuation of endothelium-dependent relaxations caused by oxidized-LDL mimicked the
endothelial dysfunction found in ApoE(-/-) mice. These results are consistent with
the suggestion that oxidized-LDL has an important role in the pathogenesis of endothelial
NO dysfunction associated with hyperlipidemia and atherosclerosis in these mice.