Basolateral Na+/H+ exchange maintains potassium secretion during diminished sodium transport in the rabbit cortical collecting duct

Basolateral Na+/H+ exchange maintains potassium secretion during diminished sodium transport in the rabbit cortical collecting duct
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DOI:
10.1038/ki.2008.447
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发表时间:
2009-01-01
影响因子:
19.6
通讯作者:
Giebisch, Gerhard
Giebisch, Gerhard
中科院分区:
医学1区
文献类型:
--
作者:
Muto, Shigeaki;Tsuruoka, Shuichi;Giebisch, Gerhard

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通过提高浴钾或管腔钠刺激离体兔皮质集管基底外侧Na+K+- atp酶,可增加钾分泌、钠吸收及其根尖传导。在这里,我们确定了刺激Na+K+- atp酶对钾分泌的影响,而不进行腔内钠运输。在不加管腔钠的情况下,将浴钾浓度从2.5 mm急剧升高至8.5mM,基底外侧膜和经上皮电压去极化,同时增加主细胞的经上皮、基底外侧和根尖膜电导。部分根尖膜阻力和细胞pH升高。净钾分泌虽然减少,但仍保持不变,增加浴钾仍能增强净钾分泌,但基底侧异丙基胺(Na+/H+交换抑制剂)能减少净钾分泌。管腔伊比利亚毒素是一种钙激活的大电导钾(BK)通道的特异性抑制剂,在存在和不存在管腔钠的情况下都会损害钾的分泌。相比之下,伊比利亚毒素不影响腔内钠转运。我们得出结论,在钠供应受损时,皮质集管中的基底外侧Na+/H+交换在维持钾分泌中起重要作用,而BK通道有助于钾的分泌
Stimulation of the basolateral Na+K+-ATPase in the isolated perfused rabbit cortical collecting duct by raising either bath potassium or lumen sodium increases potassium secretion, sodium absorption and their apical conductances. Here we determined the effect of stimulating Na+K+-ATPase on potassium secretion without luminal sodium transport. Acutely raising bath potassium concentrations from 2.5 to 8.5mM, without luminal sodium, depolarized the basolateral membrane and transepithelial voltages while increasing the transepithelial, basolateral and apical membrane conductances of principal cells. Fractional apical membrane resistance and cell pH were elevated. Net potassium secretion was maintained albeit diminished and was still enhanced by raising bath potassium, but was reduced by basolateral ethylisopropylamiloride, an inhibitor of Na+/H+ exchange. Luminal iberitoxin, a specific inhibitor of the calcium-activated big-conductance potassium (BK) channel, impaired potassium secretion both in the presence and absence of luminal sodium. In contrast, iberitoxin did not affect luminal sodium transport. We conclude that basolateral Na+/H+ exchange in the cortical collecting duct plays an important role in maintaining potassium secretion during compromised sodium supplies and that BK channels contribute to potassium