Abstract
K+ channels of the alveolar epithelium control the driving force acting on the ionic and solvent flow through the cell membranecontributing to the maintenance of cell volume and the constitution of epithelial lining fluid. In the present work, we analyze the effect of the Cl- channelinhibitors: (4-[(2-butyl-6,7-dichloro-2-cyclopentyl-2,3-dihydro-1-oxo-inden-5-yl)oxy] butanoic acid (DCPIB) and 9-anthracenecarboxylic acid (9-AC) on the total current in a type II pneumocytes (A549 cell line) model by patch clamp, immunocytochemical, and gene knockdown techniques. We noted that DCPIB and 9-AC promote the activation ofK conductance. In fact, they significantly increase the intensity of the current and shift its reversal potential to values more negative than the control. By silencing outward rectifier channel in its anoctamin 6 portion, we excluded a direct involvement of Cl- ions in modulation of IK and, by means of functional tests with its specific inhibitor spadin, we identifiedthe TREK-1 channel as the presumable target of both drugs. Asthe activity of TREK-1 has a key role for the correct functioning of the alveolar epithelium, the identification of DCPIB and 9-AC molecules as its activatorssuggests their possible use to build new pharmacological tools for the modulation of this channel.
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