Activation of renal outer medullary potassium channel in the renal distal convoluted tubule by high potassium diet.
- Author:
Xue LI
1
;
Peng-Hui LI
2
;
Yu XIAO
2
;
Kun ZHAO
2
;
Hong-Ye ZHAO
2
;
Chang-Zhu LU
2
;
Xiao-Juan QI
2
;
Rui-Min GU
3
Author Information
1. Department of Physiology, Qiqihar Medical College, Qiqihar 161000, China. lixue_0720@163.com.
2. Department of Physiology, Qiqihar Medical College, Qiqihar 161000, China.
3. Department of Pharmacology, Harbin Medical University, Harbin 150081, China.
- Publication Type:Journal Article
- MeSH:
Potassium Channels, Inwardly Rectifying/metabolism*;
Kidney Tubules, Distal/metabolism*;
Potassium/metabolism*;
Epithelial Sodium Channels/metabolism*;
Diet
- From:
Acta Physiologica Sinica
2023;75(2):188-196
- CountryChina
- Language:Chinese
-
Abstract:
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.
