Potassium conductances in tracheal epithelium activated by secretion and cell swelling.

Increased basolateral membrane K conductance accompanies stimulation of Cl secretion across canine trachea. To assess the K conductance properties, we permeabilized the apical membranes with amphotericin B and monitored the current and conductance caused by K flow across the basolateral membranes. Under basal unstimulated conditions, two K conductances could be distinguished by blockers. One was inhibited only by barium; the other was sensitive also to quinidine and lidocaine. The permeabilities of the basal conductance pathways to K and Rb were similar (PK/PRb approximately equal to 1.5). The secretory agonist, epinephrine, selectively increased the quinidine-insensitive conductance, implicating it in the Cl secretory response. Cell swelling induced a third conductance with a low permeability to Rb (PK/PRb approximately equal to 10) that was quinidine sensitive. In tissues not treated with amphotericin, neither quinidine nor Rb-for-K replacement inhibited transepithelial Cl secretion. Thus neither of the quinidine-sensitive K conductances (basal or swelling induced) contribute to the increase in basolateral K conductance during Cl secretion. Cell shrinkage inhibited all three conductances and secretion, suggesting that the initial priority of the cell is volume regulation.