The effect of high-dietary K(+) (HK) on Kir4.1/Kir5.1 and ROMK in the distal convoluted tubule (DCT) is not affected by gender and Cl(-) content of the diet.
The effect of high-dietary K(+) (HK) on Kir4.1/Kir5.1 and ROMK in the distal convoluted tubule (DCT) is not affected by gender and Cl(-) content of the diet.
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高膳食 K (HK) 对远曲小管 (DCT) 中 Kir4.1/Kir5.1 和 ROMK 的影响不受性别和饮食中 Clâ 含量的影响
DOI：
10.3389/fphys.2022.1039029
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发表时间：
2022
影响因子：
4
通讯作者：
中科院分区：
文献类型：
--
作者：
远曲小管（DCT）基底外侧钾通道由向内整流钾通道4.1 （Kir4.1）和Kir5.1组成。Kir4.1与Kir5.1相互作用形成40 pS的K+通道，这是DCT基底外侧膜中唯一表达的K+通道。此外，Kir4.1/Kir5.1异四聚体在噻嗪类药物敏感Na-Cl共转运（NCC）的表达和活性中起关键作用。除了Kir4.1/Kir5.1外，Kir1.1 （ROMK）在晚期DCT （DCT2）的顶膜中表达，并在介导上皮Na+通道（ENaC）依赖性K+排泄中起关键作用。高饮食k +摄入量（HK）刺激ROMK并抑制DCT中的Kir4.1/Kir5.1。抑制Kir4.1/Kir5.1对于HK诱导的NCC抑制至关重要，而刺激ROMK对于HK期间增加enec依赖性K+排泄很重要。我们现在使用膜片钳技术来研究性别和K+饮食中的Cl -含量是否影响hk诱导的基底外侧Kir4.1/Kir5.1抑制和hk诱导的ROMK刺激。单通道记录显示，NPo定义的DCT基底外侧40ps K+通道（Kir4.1/Kir5.1）活性在雄性小鼠为1.34 （1% KCl、正常K、NK）、0.95 （5% KCl）和1.03 （5% K+-柠檬酸盐），雌性小鼠为1.47、1.02和1.05。全细胞记录显示，雄性小鼠早期dct (DCT1) Kir4.1/ kir5.1介导的K+电流分别为1170 pA （NK）、725 pA （5% KCl）和700 pA （5% K+柠檬酸盐），而雌性小鼠早期dct （DCT1）的K+电流分别为1125 pA、674 pA和700 pA。此外，DCT的K+电流（IK）逆转电位（膜电位指标）在雄性小鼠中为-63 mV (NK), - 49 mV （5% KCl）和- 49 mV （5% K-柠檬酸盐），而在雌性小鼠中为-63 mV， - 50 mV和- 50 mV。最后，雄性小鼠DCT2 /初始连接小管（CNT）中tpnq敏感的全细胞romk电流为910 pA （NK）、1520 pA （5% KCl）和1540 pA （5% K+ -柠檬酸盐），而雌性小鼠romk介导的K+电流为1005 pA、1590 pA和1570 pA。我们得出结论，摄入HK对雄性和雌性小鼠DCT的Kir4.1/Kir5.1和DCT2/CNT的ROMK的影响是相似的。此外，HK饮食中Cl−含量对HK诱导的DCT中Kir4.1/Kir5.1的抑制和HK诱导的DCT2/CNT中ROMK的刺激没有影响。
Basolateral potassium channels in the distal convoluted tubule (DCT) are composed of inwardly-rectifying potassium channel 4.1 (Kir4.1) and Kir5.1. Kir4.1 interacts with Kir5.1 to form a 40 pS K+ channel which is the only type K+ channel expressed in the basolateral membrane of the DCT. Moreover, Kir4.1/Kir5.1 heterotetramer plays a key role in determining the expression and activity of thiazide-sensitive Na-Cl cotransport (NCC). In addition to Kir4.1/Kir5.1, Kir1.1 (ROMK) is expressed in the apical membrane of the late DCT (DCT2) and plays a key role in mediating epithelial Na+ channel (ENaC)-dependent K+ excretion. High dietary-K+-intake (HK) stimulates ROMK and inhibits Kir4.1/Kir5.1 in the DCT. Inhibition of Kir4.1/Kir5.1 is essential for HK-induced suppression of NCC whereas the stimulation of ROMK is important for increasing ENaC-dependent K+ excretion during HK. We have now used the patch-clamp-technique to examine whether gender and Cl− content of K+-diet affect HK-induced inhibition of basolateral Kir4.1/Kir5.1 and HK-induced stimulation of ROMK. Single-channel-recording shows that basolateral 40 pS K+ channel (Kir4.1/Kir5.1) activity of the DCT defined by NPo was 1.34 (1% KCl, normal K, NK), 0.95 (5% KCl) and 1.03 (5% K+-citrate) in male mice while it was 1.47, 1.02 and 1.05 in female mice. The whole-cell recording shows that Kir4.1/Kir5.1-mediated-K+ current of the early-DCT (DCT1) was 1,170 pA (NK), 725 pA (5% KCl) and 700 pA (5% K+-citrate) in male mice whereas it was 1,125 pA, 674 pA and 700 pA in female mice. Moreover, K+-currents (IK) reversal potential of DCT (an index of membrane potential) was -63 mV (NK), −49 mV (5% KCl) and −49 mV (5% K-citrate) in the male mice whereas it was -63 mV, −50 mV and −50 mV in female mice. Finally, TPNQ-sensitive whole-cell ROMK-currents in the DCT2 /initial-connecting tubule (CNT) were 910 pA (NK), 1,520 pA (5% KCl) and 1,540 pA (5% K+−citrate) in male mice whereas the ROMK-mediated K+ currents were 1,005 pA, 1,590 pA and 1,570 pA in female mice. We conclude that the effect of HK intake on Kir4.1/Kir5.1 of the DCT and ROMK of DCT2/CNT is similar between male and female mice. Also, Cl− content in HK diets has no effect on HK-induced inhibition of Kir4.1/Kir5.1 of the DCT and HK-induced stimulation of ROMK in DCT2/CNT.
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影响因子：
5.5
作者：
Lourdel, S;Paulais, M;Teulon, J
通讯作者：
Teulon, J
DOI：
10.1152/ajprenal.90527.2008
发表时间：
2009-02-01
影响因子：
4.2
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DOI：
10.1152/ajprenal.00252.2021
发表时间：
2022-01-01
影响因子：
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影响因子：
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作者：
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影响因子：
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作者：
Terker AS;Zhang C;Erspamer KJ;Gamba G;Yang CL;Ellison DH
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