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-Adrenergic regulation of amiloride-sensitive lung sodium
channels
Departments of Pediatrics and Physiology and The Center for Cell and Molecular Signaling, Emory University School of Medicine, Atlanta, Georgia 30322
We investigated the mechanism by which
cAMP increases sodium transport in lung epithelial cells. Alveolar type
II (ATII) cells have two types of amiloride-sensitive, cation channels:
a nonselective cation channel (NSC) and a highly selective channel
(HSC). Exposure of ATII cells to cAMP, 
-adrenergic agonists, or
other agents that increase adenylyl cyclase activity increased activity
of both channel types, albeit by different mechanisms. NSC open
probability (Po) increased severalfold when
exposed to terbutaline, isoproterenol, forskolin, or cAMP analogs
without any change in NSC number. In contrast, terbutaline increased
HSC number with no significant change in HSC Po.
For both channels, the effect of terbutaline was blocked by propranolol
and H-89, suggesting a protein kinase A (PKA) requirement for
-adrenergic-induced changes in channel activity. Terbutaline
increased cAMP levels in ATII cells, but intracellular calcium also
increased. Calcium sequestration with BAPTA blocked
-adrenergic-induced increases in NSC Po but
did not alter HSC activity. These observations suggest that
-adrenergic stimulation increases intracellular cAMP and activates
PKA. PKA increases HSC number and increases intracellular calcium. The increase in calcium increases NSC Po. Thus
increased cAMP levels are likely to increase lung sodium transport
regardless of which channel type is present.
single channel recording; ion transport; epithelial sodium
channels; amiloride; adenosine 3',5'-cyclic monophosphate; -adrenergic agents; alveolar type II cells
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