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高胆固醇血症诱导兔体内一种不依赖钙的一氧化氮合酶。

Induction of a calcium-independent NO synthase by hypercholesterolaemia in the rabbit.

作者信息

Lang D, Smith J A, Lewis M J

机构信息

Department of Pharmacology & Therapeutics, University of Wales College of Medicine, Heath Park, Cardiff.

出版信息

Br J Pharmacol. 1993 Feb;108(2):290-2. doi: 10.1111/j.1476-5381.1993.tb12796.x.

DOI:10.1111/j.1476-5381.1993.tb12796.x
PMID:7680590
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1907959/
Abstract

Endothelium-dependent and -independent relaxation of aortic ring preparations was assessed and nitric oxide (NO) synthase activity measured in the lung, and cerebellum of cholesterol-fed and normal rabbits. Endothelium-dependent relaxation of acetylcholine and ATP was depressed while that to the calcium ionophore, A23187, was unaltered in the cholesterol-fed group. Relaxation to sodium nitroprusside was however greater in aortae from the cholesterol-fed animals. Neither Ca(2+)-dependent nor Ca(2+)-independent NO synthase activity could be detected in aortae or hearts taken from either group of animals. Activity of both enzymes was unaltered in cerebellae from both groups of animals. Activity of the Ca(2+)-independent enzyme was however significantly greater (ca. 2 fold) in lungs from the cholesterol-fed rabbits though the activity of the Ca(2+)-dependent NO synthase was not significantly altered. This finding may account for the increased production of nitrogen oxides previously observed in this model of hypercholesterolaemia.

摘要

评估了胆固醇喂养兔和正常兔的主动脉环标本的内皮依赖性和非内皮依赖性舒张情况,并测定了肺和小脑的一氧化氮(NO)合酶活性。在胆固醇喂养组中,乙酰胆碱和ATP的内皮依赖性舒张受到抑制,而对钙离子载体A23187的舒张未改变。然而,胆固醇喂养动物的主动脉对硝普钠的舒张反应更大。在两组动物的主动脉或心脏中均未检测到钙依赖性或钙非依赖性NO合酶活性。两组动物小脑的两种酶活性均未改变。然而,胆固醇喂养兔肺中钙非依赖性酶的活性显著更高(约2倍),而钙依赖性NO合酶的活性未显著改变。这一发现可能解释了先前在该高胆固醇血症模型中观察到的氮氧化物产生增加的现象。

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本文引用的文献

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Effect of lipid feeding on endothelium dependent relaxation in rabbit aortic preparations.脂质喂养对兔主动脉制剂中内皮依赖性舒张的影响。
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Nitric oxide synthesis in endothelial cells: evidence for a pathway inducible by TNF-alpha.内皮细胞中一氧化氮的合成:肿瘤坏死因子-α诱导途径的证据。
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Atherosclerosis or lipoprotein-induced endothelial dysfunction. Potential mechanisms underlying reduction in EDRF/nitric oxide activity.动脉粥样硬化或脂蛋白诱导的内皮功能障碍。内皮依赖性舒张因子/一氧化氮活性降低的潜在机制。
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