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Received January 14, 2004
Revised February 16, 2004
Accepted after revision April 6, 2004
1 University of Dundee
2 University of Otago
* To whom correspondence should be addressed. E-mail: s.m.wilson{at}dundee.ac.uk.
The perforated patch recording technique was used to investigate the effects of dexamethasone (0.2 µM, 24 h), a synthetic glucocorticoid, upon membrane Na+ conductance (GNa) in H441 airway epithelial cells. Under zero current clamp conditions dexamethasone induced amiloride-sensitive depolarisation of membrane potential (Vm). Moreover lowering external Na+ to 10 mM, by replacement with N-methyl-D-glucammonium (NMDG+), also hyperpolarized these cells although replacing Na+ with Li+ caused a small depolarization.Despite the fact that control cells were insensitive to amiloride, NMDG+ substitution caused a small hyperpolarization and so an amiloride-insensitive cation conductance is present. Replacing Na+ with Li+ had no effect upon Vm in such cells. Voltage clamp studies of dexamethasone-treated cells showed that the reversal potential (VRev) for the amiloride-sensitive component of the membrane current was normally close to ENa. Lowering [Na+]o to 10 mM, the concentration in the pipette solution, by substitution with NMDG+ or K+ shifted VRev to a value close to zero, whilst replacing Na+ with Li+ caused a rightward shift. GNa was normally ~300 pS cell-1 in dexamethasone treated cells, but exposing these cells to a cocktail of cAMP-activating compounds for 20 min increased this conductance ~2 fold whilst having no effect upon its ionic selectivity. This increase in conductance was associated with an 18 mV depolarisation of Vm. Dexamethasone thus induces the expression of a selective Na+ conductance with a substantial permeability to Li+ that is subject to acute regulation via cAMP. These data thus suggest that selective Na+ channels underlie cAMP-regulated Na+ transport in airway epithelia.
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