Maintaining K+ balance on the low-Na+, high-K+ diet.

Maintaining K+ balance on the low-Na+, high-K+ diet.
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DOI:
10.1152/ajprenal.00330.2015
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发表时间:
2016-04
期刊:
American journal of physiology. Renal physiology
影响因子:
--
通讯作者:
Ryan J. Cornelius;Bangchen Wang;Jun Wang‐France;S. Sansom
Ryan J. Cornelius;Bangchen Wang;Jun Wang‐France;S. Sansom
中科院分区:
其他
文献类型:
--
作者:
Ryan J. Cornelius;Bangchen Wang;Jun Wang‐France;S. Sansom

文献摘要

相似文献

低Na+,高K+饮食(LNaHK)被认为是“西方”高Na+饮食更健康的选择。由于K+分泌的机制涉及远端肾单位分泌的K+与Na+的再吸收交换,因此尚不清楚K+是如何在如此低的Na+摄入量的情况下被排出的。LNaHK饮食的动物会产生碱性负荷,尿流量增加,血浆Ang II和醛固酮水平显著升高,以维持它们的K+平衡。最近的研究揭示了碱中毒、尿流、血管紧张素Ⅱ升高和醛固酮对位于主细胞和夹层细胞的两种K+通道,即肾髓外K+通道和大电导K+通道的作用机制。在这里,我们回顾了这些最新的进展。
A low-Na+, high-K+ diet (LNaHK) is considered a healthier alternative to the "Western" high-Na+ diet. Because the mechanism for K+ secretion involves Na+ reabsorptive exchange for secreted K+ in the distal nephron, it is not understood how K+ is eliminated with such low Na+ intake. Animals on a LNaHK diet produce an alkaline load, high urinary flows, and markedly elevated plasma ANG II and aldosterone levels to maintain their K+ balance. Recent studies have revealed a potential mechanism involving the actions of alkalosis, urinary flow, elevated ANG II, and aldosterone on two types of K+ channels, renal outer medullary K+ and large-conductance K+ channels, located in principal and intercalated cells. Here, we review these recent advances.