목적: Direct evidence of apical K+ secretion in the endolymphatic sac (ES) epithelium has not been reported. We tried to investigate certain K+ channels and exchangers which contribute to K+ ion transport in human ES . 방법:Human ES was harvested during acoustic tumor surgery via translabyrinthine approach. Transepithelial current was measured with scanning vibating electrode technique (SVET). To verigy K+ transporting ion channels and exchangers identified by SVET, LC- MS/MS, RT-PCR, and immunohistochemistry. 결과:The transepithelial current from human ES epithelium was blocked by 4-AP, Ba, and apamin. The current change after application of the pharmacologic agent was significant from the concentration of 10mM 4-AP , 1mM Ba, and 100nM apamin. The current was also significantly inhibited by bumatanide (10uM) and ouabain (1mM). K+ channels with this pharmacologic properties were KCNJ13, KCNJ14, KCNK2, and KCNK6. Additional K+ channels such as KCNB1, KCNC4, and KCNH1 were identified by LC-MS/MS. Finally verified K+ channnels existing in human ES epithelium by functional study, RT-PCR, and immunohistochemistry were KCNB1, KCNN2, KCNJ14, KCNK2, and KCNK6. 결론:This is the first report of apical K+ secretion in the ES epithelium. Mutiple K+ channels including inwardly rectifying, voltage-dependent, and Ca-activated K+ channels were involved in the apical K+ secretion in human ES epithelium. NKCC and Na+,K+ - ATPase provide driving forces for the K+ secretion. This apical K+ secretion in human ES epithelium is likely to play an important role in regulating relatively high K+ concentration of ES luminal fluid and endolymphatic sac potential.