Abstract
+, Cl and water from the airway lumen into the vascular space. ENaC is considered the rate limiting step in the net movement of fluid out of the alveolar space. Thus, strategies to enhance ENaC activity at the apical membrane are of interest in order to improve outcomes associated with diseases such as pneumonia and acute lung injury. ENaC in the airways is regulated by a variety of agents including G-coupled protein receptors (e.g. adrenergic, purinergic and dopaminergic), chemokines (TGF-β, TNF-α), reactive oxygen/nitrogen species (H 2 O 2 , O 2 ., NO) and hormones (glucocorticoids). The multitude of regulatory pathways highlights the importance of ENaC in the lung [3-6]. Single channel electrophysiology measurements from lung tissue demonstrate that there are two types of ENaC—highly selective cation (HSC) and non-selective cation (NSC) channels. HSC ENaC channels preferentially transport Na + (Na + /K + selectivity >40) while NSC ENaC channels are less discriminant (Na + /K + selectivity 1.4) [7]. In addition to differences in cation selectivity, HSC channels and NSC channels differ in their unitary conductance and other biophysical properties. However, they both play an important role in epithelial Na + reabsorption.
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