Functional expression of background K+ channels in rat carotid body cells.

Abstract

Oxygen‐sensing glomus cells of the carotid body (CB) express a number of K+ channels that responds to hypoxia. TASK‐like K+ channels are expressed in CB cells and have been suggested to be particularly important for hypoxia‐induced depolarization. However, it is still unclear whether the TASK‐like K+ channels in CB cells are functional correlates of TASK‐1, TASK‐3, TASK‐1/TASK‐3 heteromer, or another K+ channel. To address this issue, we studied the properties of active K+ channels in resting CB cells isolated from 6‐7 day‐old rats, and compared them with those of cloned K+ channels. Single channels were recorded from cell‐attached and inside‐out patches of CB cells. In symmetrical 150 mM KCl, ~15‐pS (TASK‐1‐like) and ~32‐pS (TASK‐3‐like) channels were present together in 90% of patches, and were inhibited by acid (pH 6.0) and methanandamide (5 μM), similar to those of cloned TASK‐1 and TASK‐3. In addition to TASK‐like channels, another acid‐sensitive K+ channel with a unitary conductance of ~30‐pS was present in ~15% of patches. Mechano‐ and fatty acid‐sensitive channels with properties of TREK‐1 and TREK‐2 were also recorded in a few patches. These results show that TASK‐like channels in CB cells are functional correlates of both TASK‐1 and TASK‐3. TREK‐1, TREK‐2 and an unidentified acid‐sensing K+ channel also present in CB cells should contribute to the background K+ current. (Funded by NIH HL054621)