Regulation of potassium (K) handling in the renal collecting duct

Abstract

This review provides an overview of the molecular mechanisms of K transport in the mammalian connecting tubule (CNT) and cortical collecting duct (CCD), both nephron segments responsible for the regulation of renal K secretion. Aldosterone and dietary K intake are two of the most important factors regulating K secretion in the CNT and CCD. Recently, angiotensin II (AngII) has also been shown to play a role in the regulation of K secretion. In addition, genetic and molecular biological approaches have further identified new mechanisms by which aldosterone and dietary K intake regulate K transport. Thus, the interaction between serum-glucocorticoid-induced kinase 1 (SGK1) and with-no-lysine kinase 4 (WNK4) plays a significant role in mediating the effect of aldosterone on ROMK (Kir1.1), an important apical K channel modulating K secretion. Recent evidence suggests that WNK1, mitogen-activated protein kinases such as P38, ERK, and Src family protein tyrosine kinase are involved in mediating the effect of low K intake on apical K secretory channels.

Fig. 1

A model of principal cell (PC) and intercalated cell (IC) illustrates the K transport under control conditions (normal K intake)

Fig. 2

A cell scheme illustrating the mechanism by which high K intake stimulates K secretion in the CCD by an aldosterone-dependent and -independent mechanisms. Solid arrow and dotted arrow indicate enhanced and diminished effect, respectively

Fig. 3

A scheme showing the role of different signaling pathways in mediating the effect of high K intake on ROMK and BK channels in the CCD. The circle with x indicates the inhibition of a particular signaling pathway

Fig. 4

A scheme showing the mechanism by which aldosterone and AngII regulate ROMK and BK channels in the CCD during low Na intake. The circle with x indicates the inhibition of a particular signaling pathway

Fig. 5

A cell scheme illustrating the mechanism by which low K intake inhibits K secretion in PC and stimulates K absorption in IC of the CCD. Solid arrow and dotted arrow indicate the enhanced and attenuated effect, respectively

Fig. 6

A scheme showing the role of different signaling pathways in mediating the effect of low K intake on ROMK and BK channels in the CCD. The circle with x indicates the inhibition of a particular signaling pathway