PMID- 20601877
OWN - NLM
STAT- MEDLINE
DCOM- 20101122
LR  - 20211203
IS  - 1473-6543 (Electronic)
IS  - 1062-4821 (Print)
IS  - 1062-4821 (Linking)
VI  - 19
IP  - 5
DP  - 2010 Sep
TI  - Regulation and function of potassium channels in aldosterone-sensitive distal 
      nephron.
PG  - 463-70
LID - 10.1097/MNH.0b013e32833c34ec [doi]
AB  - PURPOSE OF REVIEW: K channels in the aldosterone-sensitive distal nephron (ASDN) 
      participate in generating cell membrane potential and in mediating K secretion. 
      The aim of the review is to provide an overview of the recent development 
      regarding physiological function of the K channels and the novel factors which 
      modulate the K channels of the ASDN. RECENT FINDINGS: Genetic studies and 
      transgenic mouse models have revealed the physiological function of basolateral K 
      channels including inwardly rectifying K channel (Kir) and Ca-activated 
      big-conductance K channels in mediating salt transport in the ASDN. A recent 
      study shows that intersectin is required for mediating with-no-lysine kinase 
      (WNK)-induced endocytosis. Moreover, a clathrin adaptor, autosomal recessive 
      hypercholesterolemia (ARH), and an aging-suppression protein, Klothe, have been 
      shown to regulate the endocytosis of renal outer medullary potassium (ROMK) 
      channel. Also, serum-glucocorticoids-induced kinase I (SGK1) reversed the 
      inhibitory effect of WNK4 on ROMK through the phosphorylation of WNK4. However, 
      Src-family protein tyrosine kinase (SFK) abolished the effect of SGK1 on WNK4 and 
      restored the WNK4-induced inhibition of ROMK. SUMMARY: Basolateral K channels 
      including big-conductance K channel and Kir4.1/5.1 play an important role in 
      regulating Na and Mg transport in the ASDN. Apical K channels are not only 
      responsible for mediating K excretion but they are also involved in regulating 
      transepithelial Mg absorption. New factors and mechanisms by which hormones and 
      dietary K intake regulate apical K secretory channels expand the current 
      knowledge regarding renal K handling.
FAU - Wang, Wen-Hui
AU  - Wang WH
AD  - Department of Pharmacology, New York Medical College, Valhalla, New York 10595, 
      USA. wenhui_wang@nymc.edu
FAU - Yue, Peng
AU  - Yue P
FAU - Sun, Peng
AU  - Sun P
FAU - Lin, Dao-Hong
AU  - Lin DH
LA  - eng
GR  - P01 HL034300/HL/NHLBI NIH HHS/United States
GR  - R01 DK054983/DK/NIDDK NIH HHS/United States
GR  - DK54983/DK/NIDDK NIH HHS/United States
GR  - P01 HL34300/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
PL  - England
TA  - Curr Opin Nephrol Hypertens
JT  - Current opinion in nephrology and hypertension
JID - 9303753
RN  - 0 (Immediate-Early Proteins)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (KCNJ1 protein, human)
RN  - 0 (Minor Histocompatibility Antigens)
RN  - 0 (Potassium Channels)
RN  - 0 (Potassium Channels, Inwardly Rectifying)
RN  - 0 (Potassium Channels, Voltage-Gated)
RN  - 4964P6T9RB (Aldosterone)
RN  - EC 2.7.10.2 (src-Family Kinases)
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 (WNK4 protein, human)
RN  - EC 2.7.11.1 (serum-glucocorticoid regulated kinase)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - EC 3.2.1.31 (Glucuronidase)
RN  - EC 3.2.1.31 (Klotho Proteins)
RN  - I38ZP9992A (Magnesium)
SB  - IM
MH  - Aldosterone/*pharmacology
MH  - Animals
MH  - Cyclic AMP-Dependent Protein Kinases/physiology
MH  - Glucuronidase/physiology
MH  - Humans
MH  - Immediate-Early Proteins/physiology
MH  - Intracellular Signaling Peptides and Proteins
MH  - Klotho Proteins
MH  - Magnesium/metabolism
MH  - Minor Histocompatibility Antigens
MH  - Nephrons/*metabolism
MH  - Potassium Channels/*physiology
MH  - Potassium Channels, Inwardly Rectifying/physiology
MH  - Potassium Channels, Voltage-Gated/physiology
MH  - Protein Kinase C/physiology
MH  - Protein Serine-Threonine Kinases/physiology
MH  - WNK Lysine-Deficient Protein Kinase 1
MH  - src-Family Kinases/physiology
PMC - PMC4426959
MID - NIHMS684639
EDAT- 2010/07/06 06:00
MHDA- 2010/12/14 06:00
PMCR- 2015/05/11
CRDT- 2010/07/06 06:00
PHST- 2010/07/06 06:00 [entrez]
PHST- 2010/07/06 06:00 [pubmed]
PHST- 2010/12/14 06:00 [medline]
PHST- 2015/05/11 00:00 [pmc-release]
AID - 10.1097/MNH.0b013e32833c34ec [doi]
PST - ppublish
SO  - Curr Opin Nephrol Hypertens. 2010 Sep;19(5):463-70. doi: 
      10.1097/MNH.0b013e32833c34ec.