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肾脏钾生理学:饮食钾缺乏时肾脏反应的整合。

Renal potassium physiology: integration of the renal response to dietary potassium depletion.

机构信息

Renal Division, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada; Keenan Research Center, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada.

Renal Division, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada.

出版信息

Kidney Int. 2018 Jan;93(1):41-53. doi: 10.1016/j.kint.2017.08.018.

Abstract

We summarize the current understanding of the physiology of the renal handling of potassium (K), and present an integrative view of the renal response to K depletion caused by dietary K restriction. This renal response involves contributions from different nephron segments, and aims to diminish the rate of excretion of K as a result of: decreasing the rate of electrogenic (and increasing the rate of electroneutral) reabsorption of sodium in the aldosterone-sensitive distal nephron (ASDN), decreasing the abundance of renal outer medullary K channels in the luminal membrane of principal cells in the ASDN, decreasing the flow rate in the ASDN, and increasing the reabsorption of K in the cortical and medullary collecting ducts. The implications of this physiology for the association between K depletion and hypertension, and K depletion and formation of calcium kidney stones are discussed.

摘要

我们总结了目前对肾脏处理钾 (K) 生理学的理解,并提出了一种综合观点,即肾脏对饮食 K 限制引起的 K 耗竭的反应。这种肾脏反应涉及不同肾单位段的贡献,旨在通过以下方式减少 K 的排泄率:降低醛固酮敏感远端肾单位 (ASDN) 中钠的电生成性 (并增加电中性性) 重吸收率,降低 ASDN 中主细胞腔侧膜上的肾外髓质 K 通道的丰度,降低 ASDN 中的流速,并增加皮质和髓质集合管中 K 的重吸收。讨论了这种生理学对 K 耗竭与高血压之间的关联以及 K 耗竭与钙肾结石形成之间的关联的影响。

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