Question: 

The pulmonary epithelium is covered by a fluid layer, which is essential for immune defense and gas diffusion. The composition of this layer is maintained by ion transport mechanisms - including transepithelial Cl^- transport. The present study focuses on the function of basolateral Cl^- channels in pulmonary epithelia since knowledge concerning this issue is limited.

Methodology: 

Native lung preparations from Xenopuslaevis lungs were used for Ussing chamber measurements and transepithelial short-circuit currents (I_SC) were monitored in response to Cl^- channel inhibitors (DPC) and secretagouges compounds (forskolin, IBMX).

Results: 

Basolateral application of the Cl^- channel inhibitor DPC resulted in an increase of the I_SC indicating a DPC-sensitive Cl^- conductance. This observation was confirmed by establishing an apical to basolateral Cl^- gradient (with and without nystatin at apical side) or iodide gradient. Further, the effect of forskolin was increased when basolateral Cl^- channels were blocked by the simultaneous application of DPC. Activation of apical Cl^- secretion by forskolin/IBMX and subsequent DPC application resulted in a significantly reduced DPC effect. In accordance, DPC inhibition of basolateral Cl^- channels resulted in an increased apical Cl^- secretion estimated by an increased NPPB-sensitive I_SC. Furthermore, inhibition of basolateral anion exchangers responsible for Cl^- uptake resulted in a decreased DPC-sensitive current.

Conclusion: 

This study provides evidence concerning the function of basolateral Cl^- channels in Xenopus pulmonary epithelium and that these channels play a significant role in mediating apical Cl^- secretion involving a novel Cl^- recycling mechanism across the basolateral membrane.