Kerst G, Beschorner U, Unsöld B, von Hahn T, Schreiber R, Greger R, Gerlach U, Lang H J, Kunzelmann K, Bleich M
University Children's Hospital, Hoppe-Seyler-Strasse 1, 72076 Tübingen, Germany.
Pflugers Arch. 2001 Oct;443(1):146-54. doi: 10.1007/s004240100632.
KCNQ1 (KVLQT1) K+ channels play an important role during electrolyte secretion in airways and colon. KCNQ1 was cloned recently from NaCl-secreting shark rectal glands. Here we study the properties and regulation of the cloned sKVLQT1 expressed in Xenopus oocytes and Chinese hamster ovary (CHO) cells and compare the results with those obtained from in vitro perfused rectal gland tubules (RGT). The expression of sKCNQ1 induced voltage-dependent, delayed activated K+ currents, which were augmented by an increase in intracellular cAMP and Ca2+. The chromanol derivatives 293B and 526B potently inhibited sKCNQ1 expressed in oocytes and CHO cells, but had little effect on RGT electrolyte transport. Short-circuit currents in RGT were activated by alkalinization and were decreased by acidification. In CHO cells an alkaline pH activated and an acidic pH inhibited 293B-sensitive KCNQ1 currents. Noise analysis of the cell-attached basolateral membrane of RGT indicated the presence of low-conductance (<3 pS) K+ channels, in parallel with other K+ channels. sKCNQ1 generated similar small-conductance K+ channels upon expression in CHO cells and Xenopus oocytes. The results suggest the presence of low-conductance KCNQ1 K+ channels in RGT, which are probably regulated by changes in intracellular cAMP, Ca2+ and pH.
KCNQ1(KVLQT1)钾通道在气道和结肠的电解质分泌过程中发挥着重要作用。KCNQ1最近是从分泌氯化钠的鲨鱼直肠腺中克隆出来的。在此,我们研究了在非洲爪蟾卵母细胞和中国仓鼠卵巢(CHO)细胞中表达的克隆sKVLQT1的特性和调节,并将结果与体外灌注直肠腺小管(RGT)的结果进行比较。sKCNQ1的表达诱导了电压依赖性延迟激活的钾电流,细胞内cAMP和Ca2+增加时该电流增强。色满醇衍生物293B和526B可有效抑制在卵母细胞和CHO细胞中表达的sKCNQ1,但对RGT电解质转运影响很小。RGT中的短路电流在碱化时被激活,在酸化时降低。在CHO细胞中,碱性pH激活而酸性pH抑制293B敏感的KCNQ1电流。对RGT贴壁基底外侧膜的噪声分析表明存在低电导(<3 pS)钾通道,与其他钾通道并行。sKCNQ1在CHO细胞和非洲爪蟾卵母细胞中表达时产生类似的小电导钾通道。结果表明RGT中存在低电导KCNQ1钾通道,其可能受细胞内cAMP、Ca2+和pH变化的调节。