Beschreibung:
<jats:p> The cell regulatory volume decrease (RVD) response triggered by hypotonic solutions is mainly achieved by the coordinated activity of Cl<jats:sup>−</jats:sup> and K<jats:sup>+</jats:sup> channels. We now describe the molecular nature of the K<jats:sup>+</jats:sup> channels involved in the RVD response of the human bronchial epithelial (HBE) cell line 16HBE14o−. These cells, under isotonic conditions, present a K<jats:sup>+</jats:sup>current consistent with the activity of maxi K<jats:sup>+</jats:sup> channels, confirmed by RT-PCR and Western blot. Single-channel and whole cell maxi K<jats:sup>+</jats:sup> currents were readily and reversibly activated following the exposure of HBE cells to a 28% hypotonic solution. Both maxi K<jats:sup>+</jats:sup> current activation and RVD response showed calcium dependency, inhibition by TEA, Ba<jats:sup>2+</jats:sup>, iberiotoxin, and the cationic channel blocker Gd<jats:sup>3+</jats:sup> but were insensitive to clofilium, clotrimazole, and apamin. The presence of the recently cloned swelling-activated, Gd<jats:sup>3+</jats:sup>-sensitive cation channels (TRPV4, also known as OTRPC4, TRP12, or VR-OAC) was detected by RT-PCR in HBE cells. This channel, TRPV4, which senses changes in volume, might provide the pathway for Ca<jats:sup>2+</jats:sup> influx under hypotonic solutions and, consequently, for the activation of maxi K<jats:sup>+</jats:sup>channels. </jats:p>