Journal
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
Volume 458, Issue 1, Pages 157-168Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00424-008-0593-3
Keywords
Potassium transport; Potassium channel; Potassium secretion; Angiotensin; Aldosterone; K channel; Kidney
Categories
Funding
- NIH [DK 47402, DK54983, HL34100]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL034300, R23HL034100] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK054983, R01DK047402, R29DK047402] Funding Source: NIH RePORTER
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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.
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