Dietary K regulates ROMK channels in connecting tubule and cortical collecting duct of rat kidney
Dietary K regulates ROMK channels in connecting tubule and cortical collecting duct of rat kidney
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DOI：
10.1152/ajprenal.90527.2008
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发表时间：
2009-02-01
影响因子：
4.2
通讯作者：
Palmer, Lawrence G.
中科院分区：
文献类型：
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作者：
Frindt, Gustavo;Shah, Anish;Palmer, Lawrence G.
Frindt G，Shah A，Edvinsson J，Palmer LG.膳食K调节大鼠肾脏连接小管和皮质集合管中的ROMK通道。美国肾脏生理学杂志296：F347-F354，2009年。首次发表于2008年11月26日; doi：10.1152/ajprenal.90527.2008。在全细胞钳条件下，以特硫平-Q（TPRQ）敏感电流评估大鼠肾小管细胞中ROMK通道的活性。与外部的K+浓度为5 mM和内部的K+浓度为140 mM和膜电位钳位到0 mV，TPNQ阻断外向电流在主细胞的皮质集合管（CCD）外髓集合管和连接小管（CNT）。表观Ki为5.0 nM，与其与ROMK的相互作用一致。TPNQ敏感电流在接近K+平衡电位的电压下发生逆转。当移液器溶液中含有ATP时，电流降低。在CCD中，平均TPNQ敏感外向电流（I-SK）为476 +/- 48 pA/细胞在对照动物的1%KCl饮食。当动物维持高钾（10%KCl）饮食7天时，I-SK增加至1，255 +/- 140 pA，而在低钾（0.1%KCl）饮食7天时，I-SK降低至314 +/- 46 pA。在CNT中，对照组的I-SK为360 +/- 30 pA，高钾饮食组为1，160 +/- 110，低钾饮食组为166 +/- 16 pA。结果表明，ROMK通道的活性是高度调节的CCD和CNT的饮食K。
Frindt G, Shah A, Edvinsson J, Palmer LG. Dietary K regulates ROMK channels in connecting tubule and cortical collecting duct of rat kidney. Am J Physiol Renal Physiol 296: F347-F354, 2009. First published November 26, 2008; doi:10.1152/ajprenal.90527.2008.-The activity of ROMK channels in rat kidney tubule cells was assessed as tertiapin-Q (TPNQ)-sensitive current under whole cell clamp conditions. With an external K+ concentration of 5 mM and an internal K+ concentration of 140 mM and the membrane potential clamped to 0 mV, TPNQ blocked outward currents in principal cells of the cortical collecting duct (CCD) outer medullary collecting duct and connecting tubule (CNT). The apparent K-i was 5.0 nM, consistent with its interaction with ROMK. The TPNQ-sensitive current reversed at voltages close to the equilibrium potential for K+. The currents were reduced when the pipette solution contained ATP. In the CCD, the average TPNQ-sensitive outward current (I-SK) was 476 +/- 48 pA/cell in control animals on a 1% KC1 diet. I-SK increased to 1,255 +/- 140 pA when animals were maintained on a high-K (10% KC1) diet for 7 days and decreased to 314 +/- 46 pA after 7 days on a low-K (0.1% KC1) diet. In the CNT, I-SK was 360 +/- 30 pA on control, 1,160 +/- 110 on high-K, and 166 +/- 16 pA on low-K diets. The results indicate that ROMK channel activity is highly regulated by dietary K in both the CCD and the CNT.