Activation of voltage‐dependent K+ channels strongly limits hypoxia‐induced elevation of Ca2+i in rat carotid body glomus cells

摘要

Key points class="unordered" style="list-style-type:disc" id="tjp12727-list-0001">We studied the role of the large‐conductance Ca²⁺‐activated K⁺ channel (BK) and voltage‐dependent K⁺ channels (Kv) on [Ca²⁺]i responses to a wide range of hypoxia at different resting cell membrane potential (E m).BK/Kv were mostly closed at rest in normoxia. BK/Kv became basally active when cells were depolarized by elevated [KCl]o (>12 mm). Regardless of whether BK/Kv were closed or basally open, hypoxia‐induced elevation of [Ca²⁺]i was enhanced 2‐ to 3‐fold by inhibitors of BK/Kv.Hypoxia‐induced elevation of [Ca²⁺]i was enhanced ∼2‐fold by an inhibitor of Kv2, a major Kv in rat glomus cells.Hypoxia did not inhibit BK in inside‐out patches.Our study supports a scheme in which activation of BK/Kv strongly limits the magnitude of hypoxia‐induced [Ca²⁺]i rise, with Kv having a much greater effect than BK.