期刊
SEMINARS IN NEPHROLOGY
卷 33, 期 3, 页码 215-228出版社
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.semnephrol.2013.04.002
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
资金
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [RC1DK086817] Funding Source: NIH RePORTER
- NIDDK NIH HHS [RC1 DK086817] Funding Source: Medline
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据