Saito Y, Wright E M
Department of Physiology, Tohoku University School of Medicine, Miyagi, Japan.
Brain Res. 1987 Aug 11;417(2):267-72. doi: 10.1016/0006-8993(87)90451-3.
Intracellular Cl- activity (AiCl) of the bullfrog choroidal epithelium has been studied using double-barreled Cl(-)-selective microelectrodes. In bicarbonate-buffered saline, the brush-border membrane potential (VVC) was -43 mV, and AiCl was 24 mM which was twice the predicted equilibrium activity. The uphill Cl- accumulation required the presence of external Na+ and was inhibited by furosemide added to the basolateral side. Removal of HCO3- from the bath solution slightly increased AiCl. On addition of 3-isobutyl-1-methylxanthine (IBMX), VVC depolarized, and AiCl approached the equilibrium activity. It is concluded that net Cl- secretion by the choroidal epithelium is mediated by a furosemide-sensitive, Na+-coupled Cl- uptake mechanism at the basolateral border and a Cl- conductive pathway at the brush border membrane. The results suggest that intracellular cAMP either increases the Cl- conductance of the epithelial membranes and/or inhibits the NaCl co-transport mechanism.
利用双管氯离子选择性微电极研究了牛蛙脉络膜上皮细胞内的氯离子活性（AiCl）。在碳酸氢盐缓冲盐溶液中，刷状缘膜电位（VVC）为-43mV，AiCl为24mM，是预测平衡活性的两倍。氯离子的逆浓度积累需要细胞外钠离子的存在，并受到添加到基底外侧的速尿的抑制。从浴液中去除碳酸氢根离子会使AiCl略有增加。加入3-异丁基-1-甲基黄嘌呤（IBMX）后，VVC去极化，AiCl接近平衡活性。结论是脉络膜上皮细胞的净氯离子分泌是由基底外侧边界处对速尿敏感的、钠离子偶联的氯离子摄取机制以及刷状缘膜处的氯离子传导途径介导的。结果表明，细胞内的环磷酸腺苷（cAMP）要么增加上皮细胞膜的氯离子传导性，和/或抑制氯化钠共转运机制。
