Identification of the anion channel involved in volume regulation in the principal cells of rat cortical collecting duct.

阴离子外排和细胞内Ca^<2+>增加在低渗时细胞体积调节中起重要作用。本研究旨在探讨低张力诱导的细胞内Ca^<2+>升高的机制，并表征低张力在新分离的大鼠皮质集管主细胞中激活的阴离子电导。利用Fura-2荧光Ca^<2+>成像和全细胞电压钳技术，我们发现尼卡地平敏感的Ca^<2+>进入通路参与了低张力诱导的细胞内Ca^<2+>增加的机制，并且在大鼠皮质集管主细胞中，低张力刺激激活了nppb敏感/格列本脲不敏感的Cl^-电流。

Anion efflux and intracellular Ca^<2+> increase have been known to play important roles in cell volume regulation during hypotonicity. This study was carried out to explore the mechanisms of hypotonicity-induced intracellular Ca^<2+> elevation and characterize anion conductance activated by hypotonicity in the principal cells of freshly isolated rat cortical collecting ducts. Using Fura-2 fluorescence Ca^<2+> imaging and whole-cell voltage-clamp techniques, it was found that a nicardipine-sensitive Ca^<2+> entry pathway was involved in the mechanisms underlying the hypotonicity-induced intracellular Ca^<2+> increase and a NPPB-sensitive/glibenclamide-insensitive Cl^- current was activated by hypotonic stimulation in the principal cells of rat cortical collecting ducts.