Acetaldehyde and acetic acid/acetate, the active metabolites of alcohol (ethanol, EtOH), generate actions of their own ranging from behavioral, physiological, to pathological/cancerogenic effects. EtOH and acetaldehyde have been studied to some depth, whereas the effects of acetic acid have been less well explored. In this study, we investigated the effect of acetic acid on big conductance calcium-activated potassium (BK) channels present in GH3 rat pituitary tumor cells in more detail. In whole cell voltage clamp recordings, extracellular application of acetic acid increased total outward currents in a dose-dependent manner. This effect was prevented after the application of the specific BK channel blocker paxilline. Acetic acid action was pH-dependent—in whole cell current and single BK channel recordings, open probability (Po) was significantly increased by extracellular pH reduction and decreased by neutral or base pH. Acetic acid hyperpolarized the membrane potential, whereas acidic physiological solution had a depolarizing effect. Moreover, acetic acid reduced calcium (Ca²⁺) oscillations and exocytosis of growth hormone contained secretory granules from GH3 cells. These effects were partially prevented by BK inhibitors—tetraethylammonium or paxillin. In conclusion, our experiments indicate that acetic acid activates BK channels in GH3 cells which eventually contribute to acetic acid-induced membrane hyperpolarization, cessation of Ca²⁺ oscillations, and decrease of growth hormone release.

乙醛和乙酸/乙酸盐是酒精（乙醇、EtOH）的活性代谢物，它们自身会产生从行为、生理到病理/致癌作用的作用。乙醇和乙醛已得到一定程度的研究，而乙酸的影响尚未得到充分研究。在这项研究中，我们更详细地研究了乙酸对 GH3 大鼠垂体肿瘤细胞中存在的大电导钙激活钾 (BK) 通道的影响。在全细胞电压钳记录中，细胞外应用乙酸以剂量依赖性方式增加总外向电流。在应用特定的 BK 通道阻断剂 paxilline 后，这种效应被阻止。乙酸作用具有 pH 依赖性——在全细胞电流和单 BK 通道记录中，开放概率 (Po) 因细胞外 pH 值降低而显着增加，而因中性或碱性 pH 值而降低。乙酸使膜电位超极化，而酸性生理溶液具有去极化作用。此外，乙酸减少了钙（Ca ²⁺）振荡和生长激素（包含来自GH3细胞的分泌颗粒）的胞吐作用。BK 抑制剂（四乙铵或桩蛋白）可部分阻止这些作用。总之，我们的实验表明乙酸激活 GH3 细胞中的 BK 通道，最终导致乙酸诱导的膜超极化、Ca ²⁺振荡停止和生长激素释放减少。