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应用膜片箝技术的细胞贴附式与膜内向外式记录大鼠肠系膜动脉Ａ４－Ａ５分支阻力血管平滑肌（ＶＳＭ）钙激活钾通道（ＫＣａ）活动，发现外源性一氧化氮（ＮＯ）不仅在细胞贴附式下，而且在游离膜片内面向外式时均能激活ＫＣａ，在细胞贴附式，鸟苷酸环化酶抑制剂美蓝（ｍｅｔｈｙｌｅｎｅｂｌｕｅ，ＭＢ）未能阻断外源性ＮＯ激活ＫＣａ的效应。蛋白磷酸酶ＰＰＩＡ、ＰＰＩＩＡ的抑制剂ｍｉｃｒｏｃｙｓｔｉｎｅ－ＬＲ可激活ＫＣａ，并能与外源性ＮＯ的激活效应相加。提示ｃＧＭＰ／ＰＫＧ并非外源性ＮＯ激活ＫＣａ的唯一途径；抑制脱磷酸化而相对增强磷酸化也可以激活ＫＣａ活动，并能与ＮＯ激活ＫＣａ产生协同效应
Patch-clamp technique was used to record the activity of calcium-activated potassium channel (KCa) in the resistance of vascular smooth muscle cells (VSMCs) of A4-A5 in rat mesenteric artery. The results showed that exogenous nitric oxide (NO) KCa can be activated in the cell attachment mode, and outward outward in the free membrane, and in the cell attachment mode, methylene blue (MB), a guanylate cyclase inhibitor, failed to block exogenous NO activates the effects of KCa. The protein phosphatase PPIA and PPIIA inhibitor microcystine-LR can activate KCa, and can be added with exogenous NO activation. It is suggested that cGMP / PKG is not the only way for exogenous NO to activate KCa; inhibition of dephosphorylation and relative enhancement of phosphorylation also activate KCa activity and produce synergistic effect with NO activation of KCa