The Discovery, the Present State, and the Future Prospects of Endothelin
The Discovery, the Present State, and the Future Prospects of Endothelin
复制标题
内皮素的发现、现状和未来展望
DOI：
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发表时间：
1989
影响因子：
3
通讯作者：
T. Masaki
中科院分区：
文献类型：
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作者：
T. Masaki
内皮素-1（ET-1）是由血管内皮细胞产生的一种强缩血管肽。该肽具有相当独特的结构和药理学性质。ET-1在内皮细胞中产生，并且可能以类似于某些旁分泌激素的方式分泌。ET-1的升压反应主要归因于其直接的血管收缩活性。然而，肾动脉血管收缩引起的肾素释放和通过ET-1刺激中枢神经系统引起的交感神经张力升高也是升压反应的可能原因。ET-1受体和钙通道是不同的。这些受体的激活可通过磷脂酰肌醇（PI）周转刺激钙储存，诱导细胞内游离钙的瞬时增加以及通过细胞膜钙通道启动钙内流。后一种钙内流引起细胞内钙离子持续增加和挛缩。最近的实验结果表明，ET除了其心血管作用外，还可能具有心血管外活动，即，它可以是神经肽或神经分泌激素。ET-1也是细胞生长因子。
Summary Endothelin-1 (ET-1) is a potent vasoconstrictive peptide produced by endothelial cells of blood vessels. This peptide has quite a unique structure and pharmacological properties. ET-1 is produced in endothelial cells and may be secreted in a similar way to some paracrine hormones. The pressor response of ET-1 is largely ascribed to its direct vasoconstrictive activity. However, renin release induced by vasoconstriction of the renal artery and elevation of sympathetic tone via central nervous system stimulation by ET-1 are also possible causes of the pressor responses. ET-1 receptors and calcium channels are different. Activation of these receptors may stimulate calcium stores via phosphatidylinositol (PI) turnover, inducing a transient increase of intracellular free calcium as well as initiating a calcium influx via the cell membrane calcium channel. The latter calcium influx induces the sustained increase of intracellular calcium ion and contracture. Recent experimental results suggest the possibility that ET has extracardiovascular activities in addition to its cardiovascular effect, i.e., it may be a neuropeptide or a neurosecretory hormone. ET-1 is also a cell-growth factor.