PMID- 12925696
OWN - NLM
STAT- MEDLINE
DCOM- 20030924
LR  - 20181113
IS  - 0021-9738 (Print)
IS  - 0021-9738 (Linking)
VI  - 112
IP  - 4
DP  - 2003 Aug
TI  - Collecting duct-specific gene inactivation of alphaENaC in the mouse kidney does 
      not impair sodium and potassium balance.
PG  - 554-65
AB  - Aldosterone controls the final sodium reabsorption and potassium secretion in the 
      kidney by regulating the activity of the epithelial sodium channel (ENaC) in the 
      aldosterone-sensitive distal nephron (ASDN). ASDN consists of the last portion of 
      the distal convoluted tubule (late DCT), the connecting tubule (CNT), and the 
      collecting duct (CD) (i.e., the cortical CD [CCD] and the medullary CD [MCD]). It 
      has been proposed that the control of sodium transport in the CCD is essential 
      for achieving sodium and potassium balance. We have tested this hypothesis by 
      inactivating the alpha subunit of ENaC in the CD but leaving ENaC expression in 
      the late DCT and CNT intact. Under salt restriction or under aldosterone 
      infusion, whole-cell voltage clamp of principal cells of CCD showed no detectable 
      ENaC activity, whereas large amiloride-sensitive currents were observed in 
      control littermates. The animals survive well and are able to maintain sodium and 
      potassium balance, even when challenged by salt restriction, water deprivation, 
      or potassium loading. We conclude that the expression of ENaC in the CD is not a 
      prerequisite for achieving sodium and potassium balance in mice. This stresses 
      the importance of more proximal nephron segments (late DCT/CNT) to achieve sodium 
      and potassium balance.
FAU - Rubera, Isabelle
AU  - Rubera I
AD  - Institut de Pharmacologie et de Toxicologie, Rue du Bugnon 27, CH-1005 Lausanne, 
      Switzerland.
FAU - Loffing, Johannes
AU  - Loffing J
FAU - Palmer, Lawrence G
AU  - Palmer LG
FAU - Frindt, Gustavo
AU  - Frindt G
FAU - Fowler-Jaeger, Nicole
AU  - Fowler-Jaeger N
FAU - Sauter, Daniel
AU  - Sauter D
FAU - Carroll, Tom
AU  - Carroll T
FAU - McMahon, Andrew
AU  - McMahon A
FAU - Hummler, Edith
AU  - Hummler E
FAU - Rossier, Bernard C
AU  - Rossier BC
LA  - eng
GR  - DK59659/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Clin Invest
JT  - The Journal of clinical investigation
JID - 7802877
RN  - 0 (Epithelial Sodium Channels)
RN  - 0 (Homeodomain Proteins)
RN  - 0 (Hoxb7 protein, mouse)
RN  - 0 (RNA, Messenger)
RN  - 0 (Salts)
RN  - 0 (Sodium Channels)
RN  - 059QF0KO0R (Water)
RN  - 4964P6T9RB (Aldosterone)
RN  - 9NEZ333N27 (Sodium)
RN  - RWP5GA015D (Potassium)
SB  - IM
MH  - Aldosterone/blood
MH  - Animals
MH  - Electrophysiology
MH  - Epithelial Sodium Channels
MH  - Homeodomain Proteins/metabolism
MH  - Immunohistochemistry
MH  - Kidney Tubules/metabolism/*physiology
MH  - Kidney Tubules, Collecting/metabolism/*physiology
MH  - Mice
MH  - Mice, Knockout
MH  - Microscopy, Fluorescence
MH  - Potassium/metabolism
MH  - Promoter Regions, Genetic
MH  - Protein Structure, Tertiary
MH  - RNA, Messenger/metabolism
MH  - Salts/metabolism
MH  - Sodium/metabolism
MH  - Sodium Channels/*genetics/*physiology
MH  - Time Factors
MH  - Water/metabolism
PMC - PMC171384
EDAT- 2003/08/20 05:00
MHDA- 2003/09/25 05:00
PMCR- 2003/08/15
CRDT- 2003/08/20 05:00
PHST- 2003/08/20 05:00 [pubmed]
PHST- 2003/09/25 05:00 [medline]
PHST- 2003/08/20 05:00 [entrez]
PHST- 2003/08/15 00:00 [pmc-release]
AID - 112/4/554 [pii]
AID - 16956 [pii]
AID - 10.1172/JCI16956 [doi]
PST - ppublish
SO  - J Clin Invest. 2003 Aug;112(4):554-65. doi: 10.1172/JCI16956.