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高血压和动脉粥样硬化的细胞机制:缺氧诱导易卒中自发性高血压大鼠培养血管平滑肌细胞中的脂质蓄积

Cellular mechanisms of hypertension and atherosclerosis: hypoxia-induced lipid accumulation in cultured vascular smooth muscle cells from the stroke-prone spontaneously hypertensive rat.

作者信息

Shimizu S, Nara Y, Yamada K, Keiser H R, Yamori Y

机构信息

Hypertension-Endocrine Branch, National Institutes of Health, Bethesda, MD 20892.

出版信息

J Hypertens Suppl. 1988 Dec;6(4):S163-5.

PMID:3241193
Abstract

The effects of hypoxia on the lipid metabolism of cultured vascular smooth muscle cells from stroke-prone spontaneously hypertensive rats (SHRSP) were examined. The total cholesterol in smooth muscle cells cultured with hyperlipidaemic serum reached higher levels under hypoxic conditions (3.5% O2, 5.0% CO2, 91.5% N2) than under normal conditions (20% O2, 5.0% CO2, 75% N2). In normal serum, cholesterol increased slightly under hypoxic conditions. No difference was noted in cholesterol synthesis from [14C]-acetic acid. Triglyceride levels in smooth muscle cells cultured with hyperlipidaemic serum and normal serum were significantly increased compared with fetal calf serum. The increase in triglyceride levels was inhibited markedly under hypoxic conditions. Triglyceride synthesis induced by normal serum in the hypoxic cells was decreased compared with control cells. The metabolic rate of triglyceride did not differ between the two. These results indicate that hypoxic conditions accelerate the cellular uptake of cholesterol, an initial step in atherogenesis.

摘要

研究了缺氧对易卒中型自发性高血压大鼠(SHRSP)培养的血管平滑肌细胞脂质代谢的影响。在高脂血症血清中培养的平滑肌细胞,其总胆固醇在缺氧条件(3.5% O₂、5.0% CO₂、91.5% N₂)下比在正常条件(20% O₂、5.0% CO₂、75% N₂)下达到更高水平。在正常血清中,缺氧条件下胆固醇略有增加。[14C] - 乙酸胆固醇合成未见差异。与胎牛血清相比,高脂血症血清和正常血清培养的平滑肌细胞中甘油三酯水平显著升高。缺氧条件下甘油三酯水平的升高受到明显抑制。与对照细胞相比,缺氧细胞中正常血清诱导的甘油三酯合成减少。两者之间甘油三酯的代谢率没有差异。这些结果表明,缺氧条件加速了细胞对胆固醇的摄取,这是动脉粥样硬化发生的起始步骤。

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Cellular mechanisms of hypertension and atherosclerosis: hypoxia-induced lipid accumulation in cultured vascular smooth muscle cells from the stroke-prone spontaneously hypertensive rat.高血压和动脉粥样硬化的细胞机制:缺氧诱导易卒中自发性高血压大鼠培养血管平滑肌细胞中的脂质蓄积
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