NDLI: Increase in intracellular Cl− concentration by cAMP- and Ca2+-dependent stimulation of M1 collecting duct cells

Content Provider	Springer Nature Link
Author	Adam, Gabriele Ousingsawat, Jiraporn Schreiber, Rainer Kunzelmann, Karl
Copyright Year	2004
Abstract	In the lungs of cystic fibrosis (CF) patients, mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) lead to defective Cl− secretion and hyperabsorption of electrolytes. This may be a an important cause for the defective mucociliary clearance in CF lungs. Previous studies have suggested that inhibition of ENaC during activation of CFTR or by purinergic stimulation could be related to an increase in the intracellular [Cl−]i. This was examined in the present study using cultured mouse M1 collecting duct cells transfected with the chloride-sensitive enhanced yellow fluorescent protein YFPV163S. Calibration experiments showed a linear decrease of YFP fluorescence intensity with increasing [Cl−]i (0–100 mM). Activation of CFTR by isobutyl-1-methylxanthine (IBMX, 100 µM) and forskolin (2 µM) increased [Cl−]i by 9.6±1.5 mM (n=35). Similarly, ATP (100 µM) increased [Cl−]i transiently by 9.5±2.2 mM (n=17). The increase in [Cl−]i was reduced by the Na+/K+/2 Cl−-cortransporter-1 (NKCC1) blocker azosemide (100 µM), the CFTR blocker SP-303 (50 µM), the blocker of Ca2+-activated Cl− channels DIDS (100 µM) or the ENaC blocker amiloride (10 µM). Changes in YFPV163S fluorescence were not due to changes in cell volume or intracellular pH. The present data thus demonstrate an increase in [Cl−]i following stimulation with secretagogues, which could participate in the inhibition of ENaC.
Starting Page	470
Ending Page	478
Page Count	9
File Format	PDF
ISSN	00316768
Journal	Pflügers Archiv
Volume Number	449
Issue Number	5
e-ISSN	14322013
Language	English
Publisher	Springer-Verlag
Publisher Date	2004-10-29
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	CFTR ENaC Intracellular chloride Purinergic stimulation Cystic fibrosis NKCC1 YFP Cl− channels Epithelial transport
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

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$Cl^{−}$transport by cystic fibrosis transmembrane conductance regulator (CFTR) contributes to the inhibition of epithelial $Na^{+}$channels (ENaCs) inXenopusoocytes co-expressing CFTR and ENaC

CFTR is activated through stimulation of purinergic P2Y2 receptors

Cl− transport by cystic fibrosis transmembrane conductance regulator (CFTR) contributes to the inhibition of epithelial Na+ channels (ENaCs) in Xenopus oocytes co-expressing CFTR and ENaC

Disruption of CFTR chloride channel alters mechanical properties and cAMP-dependent $Cl^{−}$transport of mouse aortic smooth muscle cells

The effect of ambroxol on chloride transport, CFTR and ENaC in cystic fibrosis airway epithelial cells

ENaC inhibition stimulates Cl− secretion in the mouse cortical collecting duct through an NKCC1-dependent mechanism

Purinergic regulation of CFTR and Ca(2+)-activated Cl(-) channels and K(+) channels in human pancreatic duct epithelium.

Sensitivity of chloride efflux vs. transepithelial measurements in mixed CF and normal airway epithelial cell populations.

The cystic fibrosis transmembrane conductance regulator (CFTR) inhibits ENaC through an increase in the intracellular Cl– concentration

Increase in intracellular Cl− concentration by cAMP- and Ca2+-dependent stimulation of M1 collecting duct cells

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