Volume-activated chloride currents in pancreatic duct cells

We have used the patch clamp technique to study volume-activated Cl- currents in the bicarbonate-secreting pancreatic duct cell. These currents could be elicited by a hypertonic pipette solution (osmotic gradient 20 mOsm/l), developed over about 8 min to a peak value of 91 +/- 5.8 pA/pF at 60 mV (n...

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Bibliographic Details
Published in:The Journal of membrane biology 1995-09, Vol.147 (2), p.173-183
Main Authors: Verdon, B, Winpenny, J P, Whitfield, K J, Argent, B E, Gray, M A
Format: Article
Language:English
Subjects:
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid - pharmacology
Adenosine Triphosphate - metabolism
Animals
Anions - pharmacology
Calcium - metabolism
Calcium - pharmacology
Cell Size
Chloride Channels - antagonists & inhibitors
Chloride Channels - drug effects
Chloride Channels - metabolism
Chlorides - metabolism
In Vitro Techniques
Ion Transport
Membrane Potentials
Pancreatic Ducts - cytology
Pancreatic Ducts - metabolism
Phosphorylation
Protein Kinase C - antagonists & inhibitors
Protein Kinase C - metabolism
Rats
Rats, Wistar
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Summary:We have used the patch clamp technique to study volume-activated Cl- currents in the bicarbonate-secreting pancreatic duct cell. These currents could be elicited by a hypertonic pipette solution (osmotic gradient 20 mOsm/l), developed over about 8 min to a peak value of 91 +/- 5.8 pA/pF at 60 mV (n = 123), and were inhibited by a hypertonic bath solution. The proportion of cells which developed currents increased from 15% in freshly isolated ducts to 93% if the ducts were cultured for 2 days. The currents were ATP-dependent, had an outwardly rectifying current/voltage (I-V) plot, and displayed time-dependent inactivation at depolarizing potentials. The anion selectivity sequence was: ClO4 = I = SCN > Br = NO3 > Cl > F > HCO3 > gluconate, and the currents were inhibited to a variable extent by DIDS, NPPB, dideoxyforskolin, tamoxifen, verapamil and quinine. Increasing the intracellular Ca2+ buffering capacity, or lowering the extracellular Ca2+ concentration, reduced the proportion of duct cells which developed currents. However, removal of extracellular Ca2+ once the currents had developed was without effect. Inhibiting protein kinase C (PKC) with either the pseudosubstrate PKC (19-36), calphostin C or staurosporine completely blocked development of the currents. We speculate that cell swelling causes Ca2+ influx which activates PKC which in turn either phosphorylates the Cl- channel or a regulatory protein leading to channel activation.
ISSN:0022-2631
1432-1424
DOI:10.1007/bf00233545