PMID- 12763889
OWN - NLM
STAT- MEDLINE
DCOM- 20030717
LR  - 20211203
IS  - 0077-8923 (Print)
IS  - 0077-8923 (Linking)
VI  - 986
DP  - 2003 Apr
TI  - Short-term aldosterone action on Na,K-ATPase surface expression: role of 
      aldosterone-induced SGK1?
PG  - 554-61
AB  - Aldosterone controls extracellular volume and blood pressure by regulating Na(+) 
      reabsorption across epithelial cells of the aldosterone-sensitive distal nephron 
      (ASDN). This effect is mediated by a coordinate action on the luminal channel 
      ENaC (generally rate limiting) and the basolateral Na,K-ATPase. Long-term effects 
      of aldosterone (starting within 3 to 6 hours and increasing over days) are 
      mediated by the direct and indirect induction of stable elements of the Na(+) 
      transport machinery (e.g., Na,K-ATPase alpha subunit), whereas short-term effects 
      appear to be mediated by the upregulation of short-lived elements of the 
      machinery (e.g., ENaC alpha subunit) and of regulatory proteins, such as the 
      serum- and glucocorticoid-regulated kinase SGK1. We have recently shown that in 
      cortical collecting duct (CCD) from adrenalectomized (ADX) rats, the increase in 
      Na,K-ATPase activity (approximately threefold in 3 h), induced by a single 
      aldosterone injection, can be fully accounted for by the increase in Na,K-ATPase 
      cell-surface expression. Using the model cell line mpkCCD(cl4), we showed that 
      the parallel increase in Na,K-ATPase function [assessed by Na(+) pump current 
      (I(p)) measurements] and cell-surface expression depends on transcription and 
      translation, and that it is not secondary to a change in apical Na(+) influx. As 
      a first approach to address the question whether the aldosterone-induced 
      regulatory protein SGK1 might play a role in mediating Na,K-ATPase translocation, 
      we have used the Xenopus laevis expression system. SGK1 coexpression indeed 
      increased both the Na(+) pump current and the surface expression of pumps 
      containing the rat alpha1 subunits. In summary, aldosterone controls Na(+) 
      reabsorption in the short term not only by regulating the apical cell-surface 
      expression of ENaC but also by coordinately acting on the basolateral 
      cell-surface expression of the Na,K-ATPase. Results obtained in the Xenopus 
      oocyte expression system suggest the possibility that this effect could be 
      mediated in part by the aldosterone-induced kinase SGK1.
FAU - Verrey, Francois
AU  - Verrey F
AD  - Institute of Physiology, University of Zurich, Switzerland. 
      verrey@access.unizh.ch
FAU - Summa, Vanessa
AU  - Summa V
FAU - Heitzmann, Dirk
AU  - Heitzmann D
FAU - Mordasini, David
AU  - Mordasini D
FAU - Vandewalle, Alain
AU  - Vandewalle A
FAU - Feraille, Eric
AU  - Feraille E
FAU - Zecevic, Marija
AU  - Zecevic M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Ann N Y Acad Sci
JT  - Annals of the New York Academy of Sciences
JID - 7506858
RN  - 0 (Epithelial Sodium Channels)
RN  - 0 (Immediate-Early Proteins)
RN  - 0 (Nuclear Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Sodium Channels)
RN  - 4964P6T9RB (Aldosterone)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 2.7.11.1 (serum-glucocorticoid regulated kinase)
RN  - EC 7.2.2.13 (Sodium-Potassium-Exchanging ATPase)
SB  - IM
MH  - Aldosterone/pharmacology/*physiology
MH  - Animals
MH  - Blood Pressure/physiology
MH  - Epithelial Sodium Channels
MH  - Gene Expression Regulation, Enzymologic/drug effects
MH  - Humans
MH  - Immediate-Early Proteins
MH  - Kidney/enzymology
MH  - *Nuclear Proteins
MH  - Protein Serine-Threonine Kinases/*metabolism
MH  - RNA, Messenger/genetics
MH  - Sodium Channels/physiology
MH  - Sodium-Potassium-Exchanging ATPase/genetics/*metabolism
MH  - Transcription, Genetic/drug effects
RF  - 24
EDAT- 2003/05/24 05:00
MHDA- 2003/07/18 05:00
CRDT- 2003/05/24 05:00
PHST- 2003/05/24 05:00 [pubmed]
PHST- 2003/07/18 05:00 [medline]
PHST- 2003/05/24 05:00 [entrez]
AID - 10.1111/j.1749-6632.2003.tb07253.x [doi]
PST - ppublish
SO  - Ann N Y Acad Sci. 2003 Apr;986:554-61. doi: 10.1111/j.1749-6632.2003.tb07253.x.