The mechanisms and significance of the coupled release of endothelium-derived relaxing factor (EDRF) and prostacyclin (PGI2) from endothelial cells.
The mechanisms and significance of the coupled release of endothelium-derived relaxing factor (EDRF) and prostacyclin (PGI2) from endothelial cells.
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内皮细胞内皮源性舒张因子（EDRF）和前列环素（PGI2）耦合释放的机制和意义。
DOI：
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发表时间：
1991
影响因子：
2.6
通讯作者：
G. De Nucci
中科院分区：
文献类型：
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作者：
S. Hyslop;G. De Nucci
内皮源性松弛因子 (EDRF) 和前列环素 (PGI2) 通过膜结合受体或非受体介导机制的刺激从内皮细胞共同释放。受体介导的 EDRF 和 PGI2 释放是钙依赖性的，并且似乎受到蛋白激酶 C 的负反馈调节。EDRF 和 PGI2 之间或内皮细胞内它们各自的第二信使之间的显着相互作用尚未得到最终证明。此外，尽管EDRF和PGI2在抑制血小板聚集方面具有协同作用，但几乎没有证据表明在平滑肌松弛方面存在这种协同作用。这些观察结果表明，EDRF 和 PGI2 的释放可能主要通过它们对细胞内钙水平升高的需求以及它们通过蛋白激酶 C 的调节而耦合。
Endothelium-derived relaxing factor (EDRF) and prostacyclin (PGI2) are co-released from endothelial cells by stimuli acting via membrane-bound receptors or via non-receptor mediated mechanisms. The receptor-mediated release of EDRF and PGI2 is calcium-dependent and seems to be under the negative feedback regulation of protein kinase C. Significant interactions between EDRF and PGI2 or between their respective second messengers within the endothelial cell have not yet been conclusively demonstrated. Furthermore, although EDRF and PGI2 synergize in the inhibition of platelet aggregation, there is little evidence for such synergism in smooth muscle relaxation. These observations indicate that EDRF and PGI2 release may be coupled primarily by their requirement for raised intracellular calcium levels and by their regulation through protein kinase C.