Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University, 2-2-1 Miyama Funabashi, Chiba 274-8510, Japan.
Int J Mol Sci. 2024 Aug 9;25(16):8688. doi: 10.3390/ijms25168688.
The effects of enhanced late I, a persistent component of the Na channel current, on the intracellular ion dynamics and the automaticity of the pulmonary vein cardiomyocytes were studied with fluorescent microscopy. Anemonia viridis toxin II (ATX- II), an enhancer of late I, caused increases in the basal Na and Ca concentrations, increases in the number of Ca sparks and Ca waves, and the generation of repetitive Ca transients. These phenomena were inhibited by eleclazine, a blocker of the late I; SEA0400, an inhibitor of the Na/Ca exchanger (NCX); H89, a protein kinase A (PKA) inhibitor; and KN-93, a Ca/calmodulin-dependent protein kinase II (CaMKII) inhibitor. These results suggest that enhancement of late I in the pulmonary vein cardiomyocytes causes disturbance of the intracellular ion environment through activation of the NCX and Ca-dependent enzymes. Such mechanisms are probably involved in the ectopic electrical activity of the pulmonary vein myocardium.
应用荧光显微镜技术研究增强的晚钠电流（Na 通道电流的一个持续成分）对肺静脉心肌细胞内离子动力学和自发性的影响。增强晚钠电流的海葵毒素 II（ATX-II）引起基础 Na 和 Ca 浓度增加、钙火花和钙波数量增加以及重复钙瞬变的产生。这些现象被晚钠电流阻断剂 eleclazine、Na/Ca 交换体（NCX）抑制剂 SEA0400、蛋白激酶 A（PKA）抑制剂 H89 和 Ca/钙调蛋白依赖性蛋白激酶 II（CaMKII）抑制剂 KN-93 抑制。这些结果表明，肺静脉心肌细胞中晚钠电流的增强通过激活 NCX 和 Ca 依赖性酶导致细胞内离子环境紊乱。这些机制可能参与肺静脉心肌的异位电活动。
