期刊
KIDNEY INTERNATIONAL
卷 72, 期 5, 页码 566-573出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.ki.5002369
关键词
potassium channel; aldosterone; electrolytes; ion transport; K channels
资金
- NIDDK NIH HHS [R01 DK028602] Funding Source: Medline
The kidney is the major regulator of potassium homeostasis. In addition to the ROMK channels, large conductance Ca2+-activated K+ (BK) channels are expressed in the apical membrane of the aldosterone sensitive distal nephron where they could contribute to renal K+ secretion. We studied flow-induced K+ secretion in BK channel alpha-subunit knockout (BK-/-) mice by acute pharmacologic blockade of vasopressin V-2 receptors, which caused similar diuresis in wild-type and knockout mice. However, wild-type mice, unlike the BK-/-, had a concomitant increase in urinary K+ excretion and a significant correlation between urinary flow rate and K+ excretion. Both genotypes excreted similar urinary amounts of K+ irrespective of K+ diet. This was associated, however, with higher plasma aldosterone and stronger expression of ROMK in the apical membrane of the aldosterone-sensitive portions of the distal nephron in the knockout than in the wild-type under control diet and even more so with the high-K+ diet. High-K+ intake significantly increased the renal expression of the BK channel in the wild-type mouse. Finally, despite the higher plasma K+ and aldosterone levels, BK-/-mice restrict urinary K+ excretion when placed on a low-K+ diet to the same extent as the wild-type. These studies suggest a role of the BK channel a-subunit in flow-induced K+ secretion and in K+ homeostasis. Higher aldosterone and an upregulation of ROMK may compensate for the absence of functional BK channels.
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