Am J Physiol Cell Physiol Watch the video to learn how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol (February 15, 2006). doi:10.1152/ajpcell.00134.2005
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
291/1/C122    most recent
00134.2005v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Reddy, M.M.
Right arrow Articles by Quinton, P.M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Reddy, M.M.
Right arrow Articles by Quinton, P.M.
Submitted on March 22, 2005
Accepted on February 9, 2006

Cytosolic Potassium Controls CFTR Deactivation in Human Sweat Duct

M.M. Reddy1* and P.M. Quinton1

1 Dept. of Pediatrics, UCSD School of Medicine, San Diego, California, USA

* To whom correspondence should be addressed. E-mail: mmr{at}ucsd.edu.

Absorptive epithelial cells must admit large quantities of salt (NaCl) during the transport process. How these cells avoid swelling to protect functional integrity in the face of massive salt influx is a fundamental, unresolved problem. A special preparation of the human sweat duct provides critical insights into this crucial issue. We now show that negative feedback control of apical salt influx by regulating the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel activity is key to this protection. As part of this control process, we report a new physiological role of K+ in intracellular signaling and provide the first direct evidence of acute in vivo regulation of CFTR dephosphorylation activity. We show that cytosolic [K+]([K+]c) declines as a function of increasing cellular salt (NaCl) content at the onset of absorptive activity. Declining cytosolic [K+] cause parallel deactivation of CFTR by dephosphorylation thereby limiting apical influx of Cl- (and its co-ion Na+) until [K+]c is stabilized. We surmise that [K+]c stabilizes when Na+ influx decreases to a level equal to its efflux through the basolateral Na+/K+ pump thereby preventing disruptive changes in cell volume.




This article has been cited by other articles:


Home page
 Exp PhysiolHome page
A. K. M. Shamsuddin, M. M. Reddy, and P. M. Quinton
Iontophoretic {beta}-adrenergic stimulation of human sweat glands: possible assay for cystic fibrosis transmembrane conductance regulator activity in vivo
Exp Physiol, August 1, 2008; 93(8): 969 - 981.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
T.-Y. Chen and T.-C. Hwang
CLC-0 and CFTR: Chloride Channels Evolved From Transporters
Physiol Rev, April 1, 2008; 88(2): 351 - 387.
[Abstract] [Full Text] [PDF]

Home page
 Protein Eng Des SelHome page
V. Lovato, C. Roesli, J. Ahlskog, J. Scheuermann, and D. Neri
A monoclonal antibody prevents aggregation of the NBD1 domain of the cystic fibrosis transmembrane conductance regulator
Protein Eng. Des. Sel., December 1, 2007; 20(12): 607 - 614.
[Abstract] [Full Text] [PDF]

Home page
 Proc Am Thorac SocHome page
S. M. Rowe, F. Accurso, and J. P. Clancy
Detection of Cystic Fibrosis Transmembrane Conductance Regulator Activity in Early-Phase Clinical Trials
Proceedings of the ATS, August 1, 2007; 4(4): 387 - 398.
[Abstract] [Full Text] [PDF]

Home page
 PhysiologyHome page
P. M. Quinton
Cystic Fibrosis: Lessons from the Sweat Gland
Physiology, June 1, 2007; 22(3): 212 - 225.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 1977 by the American Physiological Society.