Effect of K channel blockers on basal and beta-agonist stimulated ion transport by fetal distal lung epithelium.

To determine whether basolateral K channels play an important role in the basal and beta-agonist stimulated ion transport by fetal distal lung epithelium we harvested these cells from fetal rats (20 days gestation, term = 22 days) and studied them in Ussing chambers. Short-circuit current (Isc) fell with basal 3 mM BaCl2 (3.0 +/- 0.2 (+/- SEM) to 2.0 +/- 0.2 microA.cm-2, n = 18, p < 0.01) without affecting monolayer resistance (R = 693 +/- 57 omega.cm2). Basal quinine sulfate (1 mM) also decreased Isc (3.7 +/- 0.15 to 3.0 +/- 0.10 microA.cm-2; n = 4, p < 0.01). None of apical BaCl2 (3 mM), apical quinine (1 mM), nor bilaterally applied tetraethylammonium (10 mM), lidocaine (1 mM), or 4-aminopyridine (2 mM) decreased Isc. Cell monolayers treated with basal BaCl2 (3 mM) demonstrated an impaired ability to increase their Isc in response to the beta 2-agonist terbutaline (1 mM). Basal 3 mM BaCl2 also decreased Isc in amiloride (0.1 mM) and furosemide (1 mM) treated monolayers, indicating that barium also affected the previously described amiloride-insensitive Na transport by these cells (n = 8, p < 0.01). Together these experiments suggest that normal basolateral K channel function is required for normal and beta 2-stimulated Na transport in fetal distal lung epithelium.