AngⅡ在肾远曲小管（DCT）Kir4.1/Kir5.1通道对NaCl的转运过程中发挥重要作用。但在低钾饮食条件下，AngⅡ对Kir4.1/Kir5.1通道作用并不清楚。先前工作证实AngⅡ与AT2R结合抑制Kir4.1/Kir5.1通道的活性和钠氯同向转运体（NCC）的转运。预实验发现低钾饮食条件下，AngⅡ可以刺激Kir4.1/Kir5.1通道的开放，并且AT2R激动剂对Kir4.1/Kir5.1通道无明显影响；同时急性低钾饮食12h，DCT的钾电流仍会增强，NCC的表达增多。因此，我们推测：在低钾饮食（12h/4d）条件下，AngⅡ可能与其受体结合通过增强Kir4.1/Kir5.1通道的活性促进NCC对NaCl的重吸收。本研究借助KS-Kcnj10-/-小鼠，揭示AngII在低钾饮食时DCT水盐转运中的重要作用，为探讨防治高血压及肾小管转运异常提供新思路。

AngⅡ plays a key role in Kir4.1/Kir5.1-induced reabsorption of NaCl in the distal convoluted tubule (DCT). The mechanism of AngⅡ on Kir4.1/Kir5.1 channel in response to dietary potassium depletion is unclear. The previous study showed AT2R inhibited activity of Kir4.1/Kir5.1 and NCC in the DCT. The pre-experiment results demonstrate AngⅡ significantly stimulates the basolateral Kir4.1/Kir5.1 activity in response to dietary potassium depletion in the DCT, whereas the agonist of AT2R have no effect on the Kir4.1/Kir5.1 activity. Meanwhile, acute dietary potassium depletion(12h) also increases DCT K+ currents and the expression of total NCC. We speculate that AngⅡ via its receptors may stimulate the activity of Kir4.1/Kir5.1 and increase the reabsorption of NaCl by NCC. We plan to reveal the key role of AngⅡ in the salt and water balance regulated by in the DCT of kidney specific Kcnj10-/- in dietary potassium depletion(12h/4d), and provide a new idea for the prevention of hypertension and possible mechanism of the abnormal tubule transport.