Matsumoto P, Russell J M
Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston 77550.
Biochim Biophys Acta. 1988 Jun 22;941(2):123-9. doi: 10.1016/0005-2736(88)90172-1.
By means of the intracellular dialysis technique, we have measured 36Cl efflux from single barnacle muscle fibers and compared the effects of raising intracellular ionized calcium concentration [( Ca2+]i) to the effects of lowering intracellular pH (pHi). Lowering pHi by 1 unit or less resulted in a 20-fold stimulation of 36Cl efflux which occurred relatively rapidly and which could be inhibited by 90-95% by 4-acetamido-4'-isothio-cyanostilbene-2,2'-disulfonic acid (SITS). In contrast, raising [Ca2+]i as much as 250-fold resulted in a relatively small increase of 36Cl efflux. The small increase occurred after a long latency, developed slowly and could not be blocked or prevented by treatment with SITS. We conclude that the increase of the SITS-sensitive 36Cl efflux caused by a fall of pHi is not mediated by a rise of [Ca2+]i.
通过细胞内透析技术，我们测量了单个藤壶肌纤维的³⁶Cl外流，并比较了提高细胞内游离钙浓度[Ca²⁺]i和降低细胞内pH值（pHi）的作用。将pHi降低1个单位或更少会导致³⁶Cl外流增加20倍，这种增加相对迅速，并且可以被4-乙酰氨基-4'-异硫氰基芪-2,2'-二磺酸（SITS）抑制90 - 95%。相比之下，将[Ca²⁺]i提高多达250倍只会导致³⁶Cl外流相对较小的增加。这种小幅度增加在长时间延迟后出现，发展缓慢，并且不能被SITS处理所阻断或预防。我们得出结论，pHi下降引起的SITS敏感的³⁶Cl外流增加不是由[Ca²⁺]i升高介导的。
