Komwatana P, Dinudom A, Young J A, Cook D I
Department of Physiology, University of Sydney, New South Wales 2006, Australia.
Proc Natl Acad Sci U S A. 1996 Jul 23;93(15):8107-11. doi: 10.1073/pnas.93.15.8107.
In tight Na+-absorbing epithelial cells, the fate of Na+ entry through amiloride-sensitive apical membrane Na+ channels is matched to basolateral Na+ extrusion so that cell Na+ concentration and volume remain steady. Control of this process by regulation of apical Na+ channels has been attributed to changes in cytosolic Ca2+ concentration or pH, secondary to changes in cytosolic Na+ concentration, although cytosolic Cl- seems also to be involved. Using mouse mandibular gland duct cells, we now demonstrate that increasing cytosolic Na+ concentration inhibits apical Na+ channels independent of changes in cytosolic Ca2+, pH, or Cl-, and the effect is blocked by GDP-beta-S, pertussis toxin, and antibodies against the alpha-subunits of guanine nucleotide-binding regulatory proteins (Go). In contrast, the inhibitory effect of cytosolic anions is blocked by antibodies to inhibitory guanine nucleotide-binding regulatory proteins (Gi1/Gi2. It thus appears that apical Na+ channels are regulated by Go and Gi proteins, the activities of which are controlled, respectively, by cytosolic Na+ and Cl-.
在紧密吸收钠离子的上皮细胞中，通过阿米洛利敏感的顶端膜钠离子通道进入细胞的钠离子的去向与基底外侧钠离子的排出相匹配，从而使细胞内钠离子浓度和体积保持稳定。尽管细胞溶质氯离子似乎也参与其中，但通过调节顶端钠离子通道对这一过程的控制归因于细胞溶质钙离子浓度或pH值的变化，这是细胞溶质钠离子浓度变化的继发效应。利用小鼠下颌腺导管细胞，我们现在证明，增加细胞溶质钠离子浓度会抑制顶端钠离子通道，而与细胞溶质钙离子、pH值或氯离子的变化无关，并且这种效应被GDP-β-S、百日咳毒素以及针对鸟嘌呤核苷酸结合调节蛋白（Go）α亚基的抗体所阻断。相反，细胞溶质阴离子的抑制作用被针对抑制性鸟嘌呤核苷酸结合调节蛋白（Gi1/Gi2）的抗体所阻断。因此，顶端钠离子通道似乎受Go和Gi蛋白调节，它们的活性分别受细胞溶质钠离子和氯离子控制。
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