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L-arginine does not restore endothelial dysfunction in atherosclerotic rabbit aorta in vitro.

作者信息

Mügge A, Harrison D G

机构信息

Cardiovascular Center, University of Iowa College of Medicine, Iowa City.

出版信息

Blood Vessels. 1991;28(5):354-7. doi: 10.1159/000158881.

DOI:10.1159/000158881
PMID:1912602
Abstract

Bioassay studies suggest that impaired endothelium-dependent relaxation in atherosclerotic arteries is due to a reduced release of biologically active endothelium-derived relaxing factor (EDRF). We tested the hypothesis that endothelial dysfunction is caused by deficiency of the EDRF precursor L-arginine. Aortae from normal and cholesterol-fed (1%, 4 months) rabbits were excised and incubated for 1 h with 5 mM L-arginine. Pretreatment with L-arginine had no effect on the relaxation to acetylcholine in normal vessels and was without effect on the impaired response of atherosclerotic arteries to acetylcholine. This finding suggests that L-arginine deficiency is unlikely the underlying cause of impaired endothelium-dependent relaxation in the aorta of cholesterol-fed rabbits.

摘要

相似文献

1
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2
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引用本文的文献

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L-Arginine does not improve endothelium-dependent relaxation inin vitro Watanabe rabbit thoracic aorta.精氨酸不能改善兔胸主动脉在体 Watanabe 内皮依赖性舒张。
Amino Acids. 1993 Oct;5(3):403-11. doi: 10.1007/BF00806958.
3
Nitric oxide function in atherosclerosis.一氧化氮在动脉粥样硬化中的作用。
Mediators Inflamm. 1997;6(1):3-21. doi: 10.1080/09629359791875.
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Interaction of the endothelial nitric oxide synthase with the CAT-1 arginine transporter enhances NO release by a mechanism not involving arginine transport.内皮型一氧化氮合酶与CAT-1精氨酸转运体的相互作用通过一种不涉及精氨酸转运的机制增强一氧化氮的释放。
Biochem J. 2005 Mar 15;386(Pt 3):567-74. doi: 10.1042/BJ20041005.
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J Clin Invest. 1997 Nov 1;100(9):2153-7. doi: 10.1172/JCI119751.
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Insulin and the arginine paradox.胰岛素与精氨酸悖论。
J Clin Invest. 1997 Feb 1;99(3):369-70. doi: 10.1172/JCI119166.
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