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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Inhibition of MAPK stimulates the Ca2+-dependent big-conductance K channels in cortical collecting duct
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Inhibition of MAPK stimulates the Ca2+-dependent big-conductance K channels in cortical collecting duct

机译：抑制MAPK刺激皮层收集管中依赖Ca2 +的大电导K通道

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The kidney plays a key role in maintaining potassium (K) homeostasis. K excretion is determined by the balance between K secretion and absorption in distal tubule segments such as the connecting tubule and cortical collecting duct. K secretion takes place by K entering principal cells (PC) from blood side through Na+, K+-ATPase and being secreted into the lumen via both ROMK-like small-conductance K (SK) channels and Ca2+-activated big-conductance K (BK) channels. K reabsorption occurs by stimulation of apical K/H-ATPase and inhibition of K recycling across the apical membrane in intercalated cells (IC). The role of ROMK channels in K secretion is well documented. However, the importance of BK channels in mediating K secretion is incompletely understood. It has been shown that their activity increases with high tubule flow rate and augmented K intake. However, BK channels have a low open probability and are mainly located in IC, which lack appropriate transporters for effective K secretion. Here we demonstrate that inhibition of ERK and P38 MAPKs stimulates BK channels in both PC and IC in the cortical collecting duct and that changes in K intake modulate their activity. Under control conditions, BK channel activity in PC was low but increased significantly by inhibition of both ERK and P38. Blocking MAPKs also increased channel open probability of BK in IC and thereby it may affect K backflux and net K absorption Thus, modulation of ERK and P38 MAPK activity is involved in controlling net K secretion in the distal nephron.
机译：肾脏在维持钾（K）动态平衡中起关键作用。钾的排泄取决于远端小管节段（例如连接小管和皮质收集管）中钾的分泌与吸收之间的平衡。 K的分泌是通过K通过血液中的Na +，K + -ATPase从血液侧进入主细胞（PC）并通过ROMK样小电导K（SK）通道和Ca2 +激活的大电导K（BK）分泌到管腔中而发生的）频道。钾的重吸收是通过刺激顶端的K / H-ATPase并抑制嵌入细胞（IC）中整个顶端膜的钾循环而实现的。 ROMK通道在K分泌中的作用已有充分文献记载。但是，BK通道在介导K分泌中的重要性尚未完全了解。已经表明，它们的活性随着高的肾小管流速和增加的钾摄入而增加。但是，BK通道的开放概率较低，并且主要位于IC中，而IC缺乏有效的K分泌的合适转运蛋白。在这里，我们证明抑制ERK和P38 MAPKs会刺激皮层收集管中PC和IC中的BK通道，并且钾摄入的变化调节了它们的活性。在控制条件下，PC中的BK通道活性较低，但通过抑制ERK和P38显着增加。阻断MAPKs也增加了BK在IC中的通道开放可能性，从而可能影响钾的返流和净K吸收。因此，调节ERK和P38 MAPK活性与控制远端肾单位的净K分泌有关。

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