Regulation of Renal Potassium Secretion: Molecular Mechanisms

被引:59
作者
Welling, Paul A. [1 ]
机构
[1] Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA
关键词
ROMK; BK; potassium channel; kidney; aldosterone; kaliuresis; hyperkalemia; hypokalemia; pseudohypoaldosteronism type II; WNK kinase; SGK-1; Src kinase; thiazide; ARH; endocytosis; Golgi; trafficking; endoplasmic reticulum; CORTICAL-COLLECTING DUCT; NA+-CL-COTRANSPORTER; MAXI-K CHANNELS; ALDOSTERONE-INDUCED KINASE; EPITHELIAL SODIUM-CHANNEL; DISTAL CONVOLUTED TUBULE; SURFACE EXPRESSION; LARGE-CONDUCTANCE; BK CHANNEL; ANGIOTENSIN-II;
D O I
10.1016/j.semnephrol.2013.04.002
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
A new understanding of renal potassium balance has emerged as the molecular underpinnings of potassium secretion have become illuminated, highlighting the key roles of apical potassium channels, renal outer medullary potassium channel (ROMK) and Big Potassium (BK), in the aldosterone-sensitive distal nephron and collecting duct. These channels act as the final-regulated components of the renal potassium secretory machinery. Their activity, number, and driving forces are precisely modulated to ensure potassium excretion matches dietary potassium intake. Recent identification of the underlying regulatory mechanisms at the molecular level provides a new appreciation of the physiology and reveals a molecular insight to explain the paradoxic actions of aldosterone on potassium secretion. Here, we review the current state of knowledge in the field. (C) 2013 Published by Elsevier Inc.
引用
收藏
页码:215 / 228
页数:14
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