Endothelin in Vascular Biology
Endothelin in Vascular Biology
复制标题
血管生物学中的内皮素
DOI：
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发表时间：
1994
影响因子：
5.2
通讯作者：
T. Masaki
中科院分区：
文献类型：
--
作者：
T. Masaki
血管张力在中枢受神经元因子调节，局部受血流调节。这些反应由内源性血管活性物质调节。大约一个世纪前，贝利斯报道说，动脉内压力的增加会引起动脉被动扩张，随后动脉会在没有神经元调节的情况下收缩。后来这种效应被证明是内皮细胞依赖的。收缩是由内皮细胞释放的血管收缩性前列腺素通过激活细胞上的拉伸受体引起的。*多年来人们也知道动脉的直径是由血流量调节的。这种反应也是内皮细胞介导的。另一方面，在过去的十年中，一些论文报道了内皮细胞产生几种血管收缩剂和血管舒张剂^。^这些发现强化了血管舒张和血管收缩依赖血流机制的概念。在周围血管床中，由于内皮细胞释放松弛因子，剪应力增大后，血管直径增大。因此，剪应力降低^，^血管张力维持在控制水平。当大鼠骨骼肌血管床以恒定流速灌注时，无论血管口径的不同，剪切应力都是近似恒定的。直径越大，血流越快。而内皮受损则破坏了反馈机制，导致血管阻力增加。在这种情况下，血管床没有随着血流量的增加而扩张。当剪应力增加时，内皮细胞释放的松弛因子部分是一氧化氮收缩因子也被证实从内皮细胞中释放出来。在培养的内皮细胞上清液中发现一种内皮来源的肽能收缩因子，命名为内皮素（endothelin， ET）这种肽的产生和释放也受血流调节。产生的ET可能局部调节血管张力。本文将讨论et调控血管张力的可能机制和血管床细胞表型的转变。
Vascular tonus is regulated centrally by neuronal factors and locally by blood flow. These responses are modulated by endogenous vasoactive substances. About a century ago, Bayliss reported that an increment of pressure inside of an artery elicited passive dilation followed by a constriction of the artery without neuronal regulation.' Later this effect was demonstrated to be endothelium dependent. The constriction was induced by vasoconstrictive prostanoids released from the endothelial cells via activation of a stretch receptor on the cells.* It has also been known for many years that the caliber of the artery is regulated by blood flow. This response is also endothelium mediated. On the other hand, in the past decade, several papers have reported that endothelial cells produce several vasoconstrictors and vasodilator^.^ Those findings reinforced the concept of a flow-dependent mechanism of vasodilation and vasoconstriction. In peripheral vascular beds, increase in shear stress is followed by increase in the diameter resulting from release of the relaxing factor from endothelium. Consequently, the shear stress decrease^,^ and vascular tonus is maintained at the control level. When the vascular beds of rat skeletal muscle were perfused with constant flow rate, shear stress was approximately constant regardless of the difference of the caliber of blood vessels. The larger the diameter, the more rapidly the bloodstream flows. Impairment of endothelium, however, abolished the feedback mechanism, resulting in an increase in vascular resistance. The vascular beds did not dilate in response to the increase in blood flow in this case. The relaxing factor released from endothelium in response to an increase in shear stress is partly nitric oxide.5 Constricting factor(s) were also demonstrated to be released from endothelial cells. An endothelium-derived peptidergic constricting factor was identified in the supernatant of the cultured endothelial cells, and named endothelin (ET).6 Production and release of this peptide are also regulated by blood flow. The ET produced probably regulates locally the vascular tonus. In this article, possible mechanisms of ET-regulated vascular tonus and transition of phenotypes of the cells in vascular beds will be discussed.
内皮素异肽对 fos 和 jun 基因表达以及 AP-1 顺式元件活性的差异调节。
DOI：
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发表时间：
1992
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Simonson,MS;Jones,JM;Dunn,MJ
通讯作者：
Dunn,MJ
通过rat-1成纤维细胞的v-src转化选择性扩增内皮素刺激的肌醇1,4,5-三磷酸和钙信号传导。
DOI：
--
发表时间：
1992
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Mattingly,RR;Wasilenko,WJ;Woodring,PJ;Garrison,JC
通讯作者：
Garrison,JC
影响因子：
--
作者：
JANAKIDEVI, K;FISHER, MA;MALIK, AB
通讯作者：
MALIK, AB