Li Xue, Li Peng-Hui, Xiao Yu, Zhao Kun, Zhao Hong-Ye, Lu Chang-Zhu, Qi Xiao-Juan, Gu Rui-Min
Department of Physiology, Qiqihar Medical College, Qiqihar 161000, China.
Department of Pharmacology, Harbin Medical University, Harbin 150081, China.
Sheng Li Xue Bao. 2023 Apr 25;75(2):188-196.
Renal outer medullary potassium (ROMK) channel is an important K excretion channel in the body, and K secreted by the ROMK channels is most or all source of urinary potassium. Previous studies focused on the ROMK channels of thick ascending limb (TAL) and collecting duct (CD), while there were few studies on the involvement of ROMK channels of the late distal convoluted tubule (DCT2) in K excretion. The purpose of the present study was mainly to record the ROMK channels current in renal DCT2 and observe the effect of high potassium diet on the ROMK channels by using single channel and whole-cell patch-clamp techniques. The results showed that a small conductance channel current with a conductance of 39 pS could be recorded in the apical membrane of renal DCT2, and it could be blocked by Tertiapin-Q (TPNQ), a ROMK channel inhibitor. The high potassium diet significantly increased the probability of ROMK channel current occurrence in the apical membrane of renal DCT2, and enhanced the activity of ROMK channel, compared to normal potassium diet (P < 0.01). Western blot results also demonstrated that the high potassium diet significantly up-regulated the protein expression levels of ROMK channels and epithelial sodium channel (ENaC), and down-regulated the protein expression level of Na-Cl cotransporter (NCC). Moreover, the high potassium diet significantly increased urinary potassium excretion. These results suggest that the high potassium diet may activate the ROMK channels in the apical membrane of renal DCT2 and increase the urinary potassium excretion by up-regulating the expression of renal ROMK channels.
肾外髓质钾离子（ROMK）通道是体内重要的钾排泄通道，由ROMK通道分泌的钾是尿钾的大部分或全部来源。以往研究主要集中在髓袢升支粗段（TAL）和集合管（CD）的ROMK通道，而关于远曲小管末端（DCT2）的ROMK通道参与钾排泄的研究较少。本研究的主要目的是利用单通道和全细胞膜片钳技术记录肾DCT2中的ROMK通道电流，并观察高钾饮食对ROMK通道的影响。结果显示，在肾DCT2的顶端膜可记录到电导为39 pS的小电导通道电流，且该电流可被ROMK通道抑制剂特律平-Q（TPNQ）阻断。与正常钾饮食相比，高钾饮食显著增加了肾DCT2顶端膜ROMK通道电流出现的概率，增强了ROMK通道的活性（P<0.01）。蛋白质免疫印迹结果还表明，高钾饮食显著上调了ROMK通道和上皮钠通道（ENaC）的蛋白表达水平，下调了氯化钠共转运体（NCC）的蛋白表达水平。此外，高钾饮食显著增加了尿钾排泄。这些结果提示，高钾饮食可能通过上调肾ROMK通道的表达来激活肾DCT2顶端膜的ROMK通道，增加尿钾排泄。
