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通过对内皮依赖性松弛作用机制的探讨，作者指出，除一氧化氮（NO）外，另有一种不依赖于cGMP的内皮衍生的超极化因子（EDHF）参与内皮依赖性扩血管作用，其超极化及松弛作用的机制可能与钙依赖性钾通道的开放有关。除NO和前列环素（PGI2）外，H2O2、花生四烯酸的非PG类代谢物及细胞色素P450等都可能是EDHF。EDHF在正常血管内皮依赖性松弛作用中的影响较小，可能不是一个重要的原始介质，但在某些疾病中，当NO的生成和利用受到干扰时，EDHF机制可能有特殊重要意义。
Through the study of the mechanism of endothelium-dependent relaxation, the authors point out that in addition to nitric oxide (NO), another endothelial-derived hyperpolarizing factor (EDHF) that is independent of cGMP is involved in endothelium-dependent vasodilation. Hyperpolarization and relaxation mechanism may be related to the opening of calcium-dependent potassium channels. In addition to NO and PGI2, H2O2, non-PG arachidonic acid metabolites and cytochrome P450 may be EDHF. EDHF may play a minor role in normal endothelium-dependent relaxation and may not be an important original mediator, but EDHF may be of particular importance in some diseases where NO production and utilization are disrupted.