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一氧化氮（NO）是主要的内皮衍生松弛因子（EDRF），通过激活鸟苷酸环化酶、使它的产物cGMP累积，以及激活几种依赖于cGMP的细胞内过程，包括通过cGMP依赖性蛋白激酶对钾通道的激活而松弛平滑肌细胞。作者提出的证据认为，外源性NO和组织所产生的EDRF两者在缺乏所需要的cGMP的、无细胞膜片钳位上，能直接激活单个Ca2+依赖性钾通道（Kca+）。在用亚甲蓝抑制鸟苷酸环化酶的条件下，NO能持续使兔主动脉显著舒张，这种舒张作用被一种专一性的Kca+通道抑制剂charybdotoxin所阻断。这些研究表明，NO对Kca+通道有一种直接激活作用。
Nitric oxide (NO) is the major endothelial derived relaxor (EDRF) that accumulates its product cGMP by activating guanylate cyclase and activates several cGMP-dependent cellular processes, including through cGMP-dependent Protein kinase relaxes smooth muscle cells by activating potassium channels. The authors suggest that both exogenous NO and tissue-derived EDRF directly activate a single Ca 2+ -dependent potassium channel (Kca +) in cell-free patch-clamps that lack the required cGMP. In the case of guanylate cyclase inhibition with methylene blue, NO sustained diastolic significant in the aorta of rabbits, which is blocked by a specific Kca + channel inhibitor, charybdotoxin. These studies show that NO has a direct activation of Kca + channels.