Duncan G, Dart C, Croghan P C, Gandolfi S A
Biomedical Research Centre, School of Biological Sciences, University of East Anglia, Norwich, U.K.
Exp Eye Res. 1992 Jun;54(6):941-6. doi: 10.1016/0014-4835(92)90158-o.
36Cl- efflux was studied in the isolated rat lens under two conditions that are known to decrease internal pH. The first follows exposure to a pulse of ammonium chloride (50 mM) and the second accompanies exposure to an acidified propionate (20 mM) solution. Under acidifying conditions, a stimulation in 36Cl- efflux was observed, that was abolished on removing external Na+ and also on removing external Cl- and HCO3-. In the absence of external Cl-, the presence of HCO3- (16 mM) resulted in an increase in 36Cl- efflux during internal acidification. In the absence of internal acidification, the addition of 0.1 mM dibutyrylcAMP or 0.5 mM IBMX to the external medium produced a rapid increase in 36Cl- efflux. This stimulation was reduced by 0.2 mM SITS. Neither cAMP or IBMX had any significant effect on the electrical resistance of the lens membranes. It is suggested that a coupled SITS-sensitive, Na(+)-Cl(-)-H(+)-HCO3- exchange mechanism is activated when the lens internal pH falls and further that cAMP may play a role in regulating this mechanism.
在已知会降低细胞内pH值的两种条件下,对分离出的大鼠晶状体中的³⁶Cl⁻外流进行了研究。第一种情况是在暴露于氯化铵脉冲(50 mM)之后,第二种情况是在暴露于酸化丙酸盐(20 mM)溶液时。在酸化条件下,观察到³⁶Cl⁻外流增加,去除细胞外Na⁺以及去除细胞外Cl⁻和HCO₃⁻时,这种增加就会消失。在没有细胞外Cl⁻的情况下,HCO₃⁻(16 mM)的存在会导致细胞内酸化期间³⁶Cl⁻外流增加。在没有细胞内酸化的情况下,向细胞外培养基中添加0.1 mM二丁酰环磷腺苷或0.5 mM异丁基甲基黄嘌呤会使³⁶Cl⁻外流迅速增加。0.2 mM的4,4'-二异硫氰基芪-2,2'-二磺酸可降低这种增加。环磷腺苷或异丁基甲基黄嘌呤对晶状体膜的电阻均无任何显著影响。研究表明,当晶状体细胞内pH值下降时,一种对4,4'-二异硫氰基芪-2,2'-二磺酸敏感的、耦合的Na⁺-Cl⁻-H⁺-HCO₃⁻交换机制被激活,并且进一步表明环磷腺苷可能在调节这一机制中发挥作用。