Intracellular Ca2+ does not activate the SITS-sensitive anion transporter in barnacle muscle.
Intracellular Ca2+ does not activate the SITS-sensitive anion transporter in barnacle muscle.
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细胞内 Ca2 不会激活藤壶肌中 SITS 敏感的阴离子转运蛋白。
DOI：
10.1016/0005-2736(88)90172-1
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Russell,JM
中科院分区：
文献类型：
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作者：
Matsumoto,P;Russell,JM
通过细胞内透析技术，我们测量了单个藤壶肌纤维的 36 Cl 流出量，并比较了提高细胞内离子钙浓度 ([Ca2+]i) 的效果与降低细胞内 pH (pHi) 的效果。 pHi 降低 1 个单位或更少会导致 36 Cl 流出量增加 20 倍，这种流出相对较快，并且可以被 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic Acid (SITS) 抑制 90-95%。相反，将[Ca 2 ] ia 提高多达250倍导致36 Cl流出量相对较小的增加。这种小幅增加是在长时间潜伏期后发生的，发展缓慢，并且不能通过 SITS 治疗来阻止或预防。我们得出的结论是，pHii 下降引起的 SITS 敏感 36Cl 流出量增加不是由 [Ca2+]i 上升介导的。
By means of the intracellular dialysis technique, we have measured36Cl 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 pHiby 1 unit or less resulted in a 20-fold stimulation of36Cl efflux which occurred relatively rapidly and which could be inhibited by 90–95% by 4-acetamido-4′-isothiocyanostilbene-2,2′-disulfonic acid (SITS). In contrast, raising [Ca2]ias much as 250-fold resulted in a relatively small increase of36Cl 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-sensitive36Cl efflux caused by a fall of pHiis not mediated by a rise of [Ca2+]i.