Activation of protein kinase C inhibits potassium currents in cultured endothelial cells.
Activation of protein kinase C inhibits potassium currents in cultured endothelial cells.
复制标题
蛋白激酶 C 的激活会抑制培养的内皮细胞中的钾电流。
DOI：
10.1159/000139289
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发表时间：
1995
期刊：
影响因子：
3.1
通讯作者：
Daniel,EE
中科院分区：
文献类型：
--
作者：
Zhang,H;Weir,B;Daniel,EE
用全细胞膜片钳技术研究了蛋白激酶C对内皮细胞钾通道的作用。蛋白激酶C的激活佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）和佛波醇12，13-二丁酸酯（PDBu），但不是佛波醇12-单肉豆蔻酸酯（PMM），佛波醇酯的无活性类似物，抑制外向钙依赖性钾电流。PMA和PDBu的抑制作用可被激酶抑制剂H-7逆转。肌浆网钙泵抑制剂Cyclopiazonic acid和释放内皮源性舒张因子的新型血管扩张剂LP-805激活了外向钙依赖性钾传导。PMA和PDBu，但不是PMM，减少由cyclopiazonic酸和LP-805诱导的外向电导。PMA和PDBu对钾电流的这些作用可能通过离子通道的磷酸化或通过降低细胞内钙浓度来介导。
The effect of protein kinase C on potassium channels in cultured endothelial cells was investigated by using whole-cell patch-clamp techniques. Activation of protein kinase C by phorbol 12-myristate 13-acetate (PMA) and phorbol 12,13-dibutyrate (PDBu), but not phorbol 12-monomyristate (PMM), an inactive analogue of phorbol esters, depressed an outward calcium-dependent potassium current. The inhibitory actions of PMA and PDBu could be reversed by the kinase inhibitor H-7. Cyclopiazonic acid, an inhibitor of the sarco-plasmic reticulum calcium pump, and LP-805, a novel vasodilator which also releases endothelium-derived relaxing factors, activated the outward calcium-dependent potassium conductance. PMA and PDBu, but not PMM, reduced the outward conductance induced by cyclopiazonic acid and LP-805. These effects of PMA and PDBu on potassium currents may be mediated either by phosphorylation of ion channels, or by decreasing intracellular calcium concentration.