Suzuki M, Takahashi K, Sakai O
Department of Pharmacology, Jichi Medical University, Tochigi, Japan.
J Membr Biol. 1994 Jul;141(1):43-50. doi: 10.1007/BF00232872.
Ca(2+)-activated K+ channels play an important role in Ca2+ signal transduction and may be regulated by mechanisms other than a direct effect of Ca2+. Inside-out patches of the apical membrane of confluent transformed rabbit cortical collecting duct cells cultured on collagen were subjected to patch clamp analysis. Two types of K+ channel, of medium and high conductance, were observed. The latter channel was characterized by a K+/Na+ permeability ratio of 10, an inwardly rectified current, a conductance of 80 pS at 0 mV, and an open probability dependent on both voltage and Ca2+. Guanosine 5'-triphosphate (GTP) but not a guanosine 5'-diphosphate (GDP) analogue, adenosine 5'-triphosphate (ATP), cytidine 5'-triphosphate (CTP), or inosine 5'-triphosphate (ITP), inhibited the activity of this Ca(2+)-activated K+ channel. The inhibitory effect of GTP was dose dependent, with a 50% inhibitory concentration of 10(-5) M in the absence of Mg2+. In the presence of Mg2+ (1 mM), which is required for the binding of GTP to G proteins, the 50% inhibitory concentration decreased to 3 x 10(-12) M. Pertussis toxin or cholera toxin (each at 10 ng/ml) did not prevent the inhibitory effect of GTP. After removal of GTP from the medium bathing an inhibited channel, subsequent application of Ca2+ failed to activate the channel. Ca(2+)-activated K+ channels of smooth muscle cells and proximal tubule cells did not respond to GTP. Thus, the Ca(2+)-activated K+ channel in the apical membrane of collecting duct cells is inhibited by GTP, which appears to exert its effect via a G protein that is insensitive to both cholera and pertussis toxins.
钙离子激活的钾离子通道在钙离子信号转导中起重要作用,并且可能受除钙离子直接作用以外的机制调控。对培养在胶原上的汇合转化兔皮质集合管细胞顶端膜的内面向外膜片进行膜片钳分析。观察到两种类型的钾离子通道,即中等电导和高电导通道。后一种通道的特征是钾离子/钠离子通透率为10,内向整流电流,在0 mV时电导为80 pS,开放概率依赖于电压和钙离子。鸟苷5'-三磷酸(GTP)而非鸟苷5'-二磷酸(GDP)类似物、腺苷5'-三磷酸(ATP)、胞苷5'-三磷酸(CTP)或肌苷5'-三磷酸(ITP)可抑制这种钙离子激活的钾离子通道的活性。GTP的抑制作用呈剂量依赖性,在无镁离子时50%抑制浓度为10⁻⁵ M。在存在GTP与G蛋白结合所需的镁离子(1 mM)时,50%抑制浓度降至3×10⁻¹² M。百日咳毒素或霍乱毒素(均为10 ng/ml)不能阻止GTP的抑制作用。从浸泡受抑制通道的培养基中去除GTP后,随后施加钙离子未能激活该通道。平滑肌细胞和近端小管细胞的钙离子激活的钾离子通道对GTP无反应。因此,集合管细胞顶端膜中的钙离子激活的钾离子通道受GTP抑制,这似乎是通过一种对霍乱毒素和百日咳毒素均不敏感的G蛋白发挥作用。