Document Detail

Purinergic-induced ion current in monolayers of C7-MDCK cells: role of basolateral and apical ion transporters.
MedLine Citation:
PMID:  12148840     Owner:  NLM     Status:  MEDLINE    
This study examines purinergic modulation of short-circuit current (I(SC)) in monolayers of C7- and C11-MDCK cells resembling principal and intercalated cells from collecting ducts. In C7 monolayers, basolateral and apical application of ATP led to similar elevation of I(SC), consisting of a transient phase with maximal I(SC) increment of approximately 10 microA/cm2 terminating in 2-3 min, and a sustained phase with maximal I(SC) less than 2 microA/cm2 and terminating in 10 min. ATP-induced I(SC) was insensitive to the presence of Na+, Cl- and inhibitors of K+ (Ba2+, charibdotoxin (ChTX), clotrimazole (CLT), apamin) and Na + (amiloride) channels in the mucosal solution. Inhibitors of Cl- channels, DIDS and NPPB, added to apical membranes at a concentration of 100 microM, did not affect ATP-induced I(SC), whereas at 500 microM, NPPB inhibited it by 70-80%. Substitution of Cl- with NO3- in serosal medium decreased ATP-induced I(SC) by 2-3-fold and elevation of [K+]o from 6 to 60 mM changed its direction. Basolateral NPPB inhibited I(SC) by 10-fold with ED50 of approximately 30 microM, whereas ChTX (50 nM) and CLT (2 microM) diminished this parameter by 30-50%. Suppression of Na+, K+, Cl- cotransport with bumetanide did not affect the transient phase of ATP-induced I(SC) and slightly diminished its sustained phase. ATP increased ouabainand bumetanide-resistant K+ (86Rb) influx across the basolateral membrane by 7-8-fold, which was partially inhibited with ChTX and CLT. ATP-treated C11 cells exhibited negligible I(SC), and their presence did not affect I(SC) triggered by ATP in C7 cells. Thus, our results show that transcellular ion current in ATP-treated C7 cells is mainly caused by the coupled function of apical and basolateral anion transporters providing transient Cl- secretion. These transporters possess different sensitivities to anion channel blocker NPBB and are under the control of basolateral K+ channels(s) inhibited by ChTX and CLT.
N Bourcier; R Grygorczyk; M Gekle; Y Berthiaume; S N Orlov
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of membrane biology     Volume:  186     ISSN:  0022-2631     ISO Abbreviation:  J. Membr. Biol.     Publication Date:  2002 Apr 
Date Detail:
Created Date:  2002-07-31     Completed Date:  2002-12-18     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0211301     Medline TA:  J Membr Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  131-43     Citation Subset:  IM    
Centre de recherche, Centre hospitalier de l'Université de Montréal-Hôtel-Dieu, Quebec, Canada.
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MeSH Terms
Adenosine Triphosphate / administration & dosage
Cell Line
Chloride Channels / metabolism*
Epinephrine / administration & dosage
Kidney Tubules, Collecting / drug effects,  metabolism*
Patch-Clamp Techniques / methods
Potassium Channels / metabolism*
Receptors, Purinergic P2 / metabolism*
Reproducibility of Results
Sensitivity and Specificity
Sodium Channels / metabolism*
Sodium-Potassium-Chloride Symporters / metabolism
Reg. No./Substance:
0/Chloride Channels; 0/Potassium Channels; 0/Receptors, Purinergic P2; 0/Sodium Channels; 0/Sodium-Potassium-Chloride Symporters; 51-43-4/Epinephrine; 56-65-5/Adenosine Triphosphate

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