PMID- 19277701
OWN - NLM
STAT- MEDLINE
DCOM- 20090724
LR  - 20220408
IS  - 1432-2013 (Electronic)
IS  - 0031-6768 (Linking)
VI  - 458
IP  - 1
DP  - 2009 May
TI  - Regulated sodium transport in the renal connecting tubule (CNT) via the 
      epithelial sodium channel (ENaC).
PG  - 111-35
LID - 10.1007/s00424-009-0656-0 [doi]
AB  - The aldosterone-sensitive distal nephron (ASDN) includes the late distal 
      convoluted tubule 2, the connecting tubule (CNT) and the collecting duct. The 
      appropriate regulation of sodium (Na(+)) absorption in the ASDN is essential to 
      precisely match urinary Na(+) excretion to dietary Na(+) intake whilst taking 
      extra-renal Na(+) losses into account. There is increasing evidence that Na(+) 
      transport in the CNT is of particular importance for the maintenance of body 
      Na(+) balance and for the long-term control of extra-cellular fluid volume and 
      arterial blood pressure. Na(+) transport in the CNT critically depends on the 
      activity and abundance of the amiloride-sensitive epithelial sodium channel 
      (ENaC) in the luminal membrane of the CNT cells. As a rate-limiting step for 
      transepithelial Na(+) transport, ENaC is the main target of hormones (e.g. 
      aldosterone, angiotensin II, vasopressin and insulin/insulin-like growth factor 
      1) to adjust transepithelial Na(+) transport in this tubular segment. In this 
      review, we highlight the structural and functional properties of the CNT that 
      contribute to the high Na(+) transport capacity of this segment. Moreover, we 
      discuss some aspects of the complex pathways and molecular mechanisms involved in 
      ENaC regulation by hormones, kinases, proteases and associated proteins that 
      control its function. Whilst cultured cells and heterologous expression systems 
      have greatly advanced our knowledge about some of these regulatory mechanisms, 
      future studies will have to determine the relative importance of the various 
      pathways in the native tubule and in particular in the CNT.
FAU - Loffing, Johannes
AU  - Loffing J
AD  - Institute of Anatomy, University of Zurich, Switzerland. 
      johannes.loffing@anatom.uzh.ch
FAU - Korbmacher, Christoph
AU  - Korbmacher C
LA  - eng
GR  - Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20090311
PL  - Germany
TA  - Pflugers Arch
JT  - Pflugers Archiv : European journal of physiology
JID - 0154720
RN  - 0 (Endosomal Sorting Complexes Required for Transport)
RN  - 0 (Epithelial Sodium Channels)
RN  - 0 (Immediate-Early Proteins)
RN  - 0 (Insulin)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (Minor Histocompatibility Antigens)
RN  - 11000-17-2 (Vasopressins)
RN  - 11128-99-7 (Angiotensin II)
RN  - 4964P6T9RB (Aldosterone)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - 9NEZ333N27 (Sodium)
RN  - EC 2.3.2.26 (Nedd4 Ubiquitin Protein Ligases)
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 2.7.11.1 (WNK Lysine-Deficient Protein Kinase 1)
RN  - EC 2.7.11.1 (WNK1 protein, human)
RN  - EC 2.7.11.1 (serum-glucocorticoid regulated kinase)
SB  - IM
MH  - Aldosterone/physiology
MH  - Angiotensin II/physiology
MH  - Animals
MH  - Endosomal Sorting Complexes Required for Transport
MH  - Epithelial Sodium Channels/chemistry/*metabolism
MH  - Homeostasis/physiology
MH  - Humans
MH  - Immediate-Early Proteins/physiology
MH  - Insulin/physiology
MH  - Insulin-Like Growth Factor I/physiology
MH  - Intracellular Signaling Peptides and Proteins
MH  - Kidney Tubules, Collecting/*metabolism
MH  - Minor Histocompatibility Antigens
MH  - Nedd4 Ubiquitin Protein Ligases
MH  - Protein Serine-Threonine Kinases/physiology
MH  - Protein Transport/drug effects
MH  - Sodium/*metabolism/urine
MH  - Ubiquitin-Protein Ligases/physiology
MH  - Ubiquitination
MH  - Vasopressins/physiology
MH  - WNK Lysine-Deficient Protein Kinase 1
RF  - 371
EDAT- 2009/03/12 09:00
MHDA- 2009/07/25 09:00
CRDT- 2009/03/12 09:00
PHST- 2009/01/14 00:00 [received]
PHST- 2009/02/22 00:00 [accepted]
PHST- 2009/02/18 00:00 [revised]
PHST- 2009/03/12 09:00 [entrez]
PHST- 2009/03/12 09:00 [pubmed]
PHST- 2009/07/25 09:00 [medline]
AID - 10.1007/s00424-009-0656-0 [doi]
PST - ppublish
SO  - Pflugers Arch. 2009 May;458(1):111-35. doi: 10.1007/s00424-009-0656-0. Epub 2009 
      Mar 11.