Journal
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
Volume 299, Issue 4, Pages F890-F897Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajprenal.00323.2010
Keywords
K loading; K depletion; ENaC; ROMK; NCC
Categories
Funding
- National Institutes of Health [DK27847, DK59659, DK54231]
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Frindt G, Palmer LG. Effects of dietary K on cell-surface expression of renal ion channels and transporters. Am J Physiol Renal Physiol 299: F890-F897, 2010. First published August 11, 2010; doi:10.1152/ajprenal.00323.2010.-Changes in apical surface expression of ion channels and transporters in the superficial rat renal cortex were assessed using biotinylation and immunoblotting during alterations in dietary K intake. A high-K diet increased, and a low-K diet decreased, both the overall and surface abundance of the beta- and gamma-subunits of the epithelial Na channel (ENaC). In the case of gamma-ENaC, the effect was specific for the 65-kDa cleaved form of the protein. The overall amount of alpha-ENAC was also increased with increasing K intake. The total expression of the secretory K+ channels (ROMK) increased with a high-K diet and decreased with a low-K diet. The surface expression of ROMK increased with high K intake but was not significantly altered by a low-K diet. In contrast, the amounts of total and surface protein representing the thiazide-sensitive NaCl cotransporter (NCC) decreased with increasing K intake. We conclude that modulation of K+ secretion in response to changes in dietary K intake involves changes in apical K+ permeability through regulation of K+ channels and in driving force subsequent to alterations in both Na delivery to the distal nephron and Na+ uptake across the apical membrane of the K+ secretory cells.
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