肾外髓钾通道(renal outer medullary potassium channel, ROMK)是内向整流钾通道超家族成员,介导肾小管上皮细胞内K+ 向小管腔的转运,在维持机体钾稳态方面发挥重要作用。其编码基因突变可引起肾功能受损,呈现以K+ 代谢紊乱为特点的II型Bartter's综合征,故ROMK 通道功能状态的改变可造成机体水、电解质和血压等内环境稳态被破坏。本文旨在概述近年肾小管顶端膜ROMK通道的相关研究进展,重点阐述 ROMK 通道的功能及其活性调控,以期为临床离子代谢紊乱等病症的预防和治疗提供新思路。

The renal outer medullary K+ channel (ROMK) is a member of the inwardly rectifying potassium channel superfamily, which mediates the transport of K+ from renal tubular epithelial cells into the tubular lumen and plays a crucial role in maintaining the body' s K+ homeostasis. Mutations in its gene can cause impaired renal function, characterized by type II Bartter's syndrome with K+ metabolic disturbances. Therefore, alternations in the functional status of ROMK channels can disrupt the transport of K+ and Na+ , as well as the homeostasis of water, electrolyte and blood pressure. Here we review recent progress regarding the ROMK channels in the apical membrane of renal tubules, focusing on their function and the regulation of activity, to provide new insights for the prevention and treatment of clinical conditions involving ion metabolic disorders.