Impact of K(+) homeostasis on net acid secretion in rat terminal inner medullary collecting duct: role of the Na,K-ATPase.
Impact of K(+) homeostasis on net acid secretion in rat terminal inner medullary collecting duct: role of the Na,K-ATPase.
复制标题
K( )稳态对大鼠终末内髓集合管净酸分泌的影响：Na,K-ATP酶的作用。
DOI：
10.1053/ajkd.2000.19115
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发表时间：
2000
期刊：
影响因子：
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通讯作者：
Wall,SM
中科院分区：
文献类型：
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作者：
Wall,SM
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For the past 50 years, the mechanism of ammonium (NH4+) transport along the collecting duct has been thought to occur through active H+secetion in parallel with the nonionic diffusion of ammonia (NH3). This model is supported by two basic experimental observations. First, NH4+secretion generally correlates with the NH3concentration gradient between the interstitium and the collecting duct lumen. This NH3gradient is generated through both luminal acidification, which reduces luminal NH3concentration, and through countercurrent multiplication, which increases interstitial NH3concentration. The result is secretion of NH3into the collecting duct lumen down its concentration gradient. Second, because NH4+permeability is low relative to that of NH3, there is significant secretion of NH3into the collecting duct lumen with minimal back-diffusion of NH4+. However, our laboratory, as well as others, has shown that this model is an oversimplification of the mechanism of NH4+transport along the collecting duct. NH4+is transported through a variety of K+transport pathways including Na,K-ATPase. K+and NH4+compete for a common extracellular binding site on Na,K-ATPase. During hypokalemia, interstitial K+concentration is reduced, which augments NH4+uptake by the Na+pump. In K+restriction, Na,K-ATPase–mediated NH4+uptake provides an important source of H+for net acid secretion and for the titration of luminal buffers in the terminal inner medullary collecting duct. This pathway contributes to the increase in NH4+excretion and metabolic alkalosis observed during hypokalemia.