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钙拮抗剂与动脉粥样硬化形成中的血管平滑肌细胞

Calcium antagonists and vascular smooth muscle cells in atherogenesis.

作者信息

Pauletto P, Sartore S, Giuriato L, Scatena M, Tonello M, Scannapieco G, Pessina A C, Dal Palù C

机构信息

Istituto di Medicina Clinica, Università di Padova, Italy.

出版信息

J Cardiovasc Pharmacol. 1992;19 Suppl 2:S8-16. doi: 10.1097/00005344-199219002-00004.

DOI:10.1097/00005344-199219002-00004
PMID:1377310
Abstract

Vascular smooth muscle cells (SMCs) play a key role in the development of atherosclerotic lesions. Vascular smooth muscle, however, does not represent a homogeneous tissue. Using myosin as a marker of the differentiation processes in development and in vascular disease, we have been able to demonstrate the existence of distinct SMC populations in rabbit aorta. In our studies, a specific SMC population of the aortic media showing an "immature" type of myosin isoform expression accounted for the majority of SMCs present in the atherosclerotic plaque. Nifedipine, a dihydropyridine-derived calcium antagonist, was able to decrease the size of this particular SMC population and to prevent the development of atherosclerotic lesions in hypercholesterolemic rabbits. Here we report about a similar effect obtained by treating hypercholesterolemic rabbits with nitrendipine, another dihydropyridine-derived calcium antagonist. This article also summarizes the main experimental and clinical studies conducted on the antiatherogenic effect of calcium antagonists and focuses on the mechanisms underlying this effect, particularly at the vascular SMC level.

摘要

血管平滑肌细胞(SMC)在动脉粥样硬化病变的发展中起关键作用。然而,血管平滑肌并非均质组织。利用肌球蛋白作为发育过程和血管疾病中分化过程的标志物,我们已能够证实兔主动脉中存在不同的SMC群体。在我们的研究中,主动脉中膜显示“不成熟”型肌球蛋白同工型表达的特定SMC群体占动脉粥样硬化斑块中存在的SMC的大多数。硝苯地平,一种二氢吡啶类钙拮抗剂,能够减小这一特定SMC群体的大小,并预防高胆固醇血症兔动脉粥样硬化病变的发展。在此我们报告用另一种二氢吡啶类钙拮抗剂尼群地平治疗高胆固醇血症兔所获得的类似效果。本文还总结了关于钙拮抗剂抗动脉粥样硬化作用的主要实验和临床研究,并着重于这种作用的潜在机制,特别是在血管SMC水平上的机制。

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Calcium antagonists and vascular smooth muscle cells in atherogenesis.钙拮抗剂与动脉粥样硬化形成中的血管平滑肌细胞
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引用本文的文献

1
Impact of nifedipine on vascular smooth muscle cell differentiation. Implications for atherogenesis.
Drugs. 1994;48 Suppl 1:1-7. doi: 10.2165/00003495-199400481-00003.