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 (I(sc)) fell with basal 3 mM BaCl2 (3.0 +/- 0.2 (+/-SEM) to 2.0 +/- 0.2 muA . CM-2, n = 18, p < 0.01) without affecting monolayer resistance (R = 693 +/- 57 OMEGA . cm2). Basal quinine sulfate (1 mM) also decreased I(sc) (3.7 +/- 0.15 to 3.0 +/- 0. 10 muA . cm-2; n = 4, p < 0.01). None of apical BaCl2 (3 mM), apical quinine (1 mM), nor bilaterally applied tetraethylammonium (10 mM), lidocaine (I mM), or 4-aminopyridine (2 mM) decreased I(sc). Cell monolayers treated with basal BaCl2 (3 mM) demonstrated an impaired ability to increase their I(sc) in response to the beta2-agonist terbutaline (I mM). Basal 3 mM BaCl2 also decreased I(sc) 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 beta2-stimulated Na transport in fetal distal lung epithelium.