Nifedipine increases cholesteryl ester hydrolytic activity in lipid-laden rabbit arterial smooth muscle cells. A possible mechanism for its antiatherogenic effect.
Nifedipine increases cholesteryl ester hydrolytic activity in lipid-laden rabbit arterial smooth muscle cells. A possible mechanism for its antiatherogenic effect.
复制标题
硝苯地平可增加富含脂质的兔动脉平滑肌细胞中胆固醇酯的水解活性。
DOI：
10.1172/jci111860
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Hajjar,DP
中科院分区：
文献类型：
--
作者：
Etingin,OR;Hajjar,DP
Calcium and cholesterol (CHOL) accumulation are characteristic features of human atherosclerotic plaques. Calcium channel blockers have been shown to increase calcium levels in myocardial cells and suppress free and esterified CHOL deposition in arteries of CHOL-fed animals. To test the hypothesis that Nifedipine alters CHOL metabolism, thereby decreasing free and esterified CHOL accumulation in smooth muscle cells (SMC), we cultured arterial SMC from rabbits fed a normal or egg-supplemented diet for 6 mo. Cultured cells were treated with 0.1 mg/liter Nifedipine every 3 d during a 1-wk experiment. Although Nifedipine significantly increased lysosomal and cytoplasmic cholesteryl ester (CE) hydrolase activity in normal SMC via increased levels of intracellular cyclic AMP, no change in total CHOL content was observed after 1 wk of Nifedipine treatment. Contrary to these observations, lipid-laden SMC demonstrated a significant 50% loss in CHOL and CE after treatment with Nifedipine, due in part to the observed increase in CE hydrolytic activities. These data support our hypothesis that Nifedipine decreases CHOL and CE accumulation in arterial SMC by increasing arterial CE hydrolysis.
