Journal
EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 424, Issue 2, Pages 141-149Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/S0014-2999(01)01140-2
Keywords
apolipoprotein-E; atherosclerosis; endothelial dysfunction; hyperlipidemia; nitric oxide (NO); LDL (low-density lipoproteins, oxidized)
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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 mug/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 muM) and the nonspecific vasodilator papaverine (100 muM) 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. (C) 2001 Elsevier Science B.V. All rights reserved.
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