Young R J, Smith T C, Levinson C
Department of Physiology, University of Texas Health Science Center, San Antonio 78284-7756.
Biochim Biophys Acta. 1993 Feb 23;1146(1):81-6. doi: 10.1016/0005-2736(93)90341-v.
Ehrlich ascites tumor cells suspended in hyposmotic solution initially swell and then shrink back towards normal volume, a process known as regulatory volume decrease (RVD). RVD is characterized by a specific loss of KCl, although the mechanism for this is currently unknown. The hypothesis that a rise in intracellular calcium ([Ca2+]i) activates calcium-sensitive ion conductances to initiate RVD was investigated. The results indicate that in the Ehrlich cell no rise in [Ca2+]i occurs when the extracellular osmolality is reduced from 300 mosM to 180 mosM. These findings were substantiated by the lack of sensitivity of RVD to the Ca(2+)-sensitive K+ channel blockers charybdotoxin (CTX) and nifedipine. In contrast, the ionophore ionomycin induced a cell shrinkage that was sensitive to CTX and nifedipine indicating that a rise in [Ca2+]i could play a role in cell volume reduction but that this occurred by a mechanism different from that observed in RVD. The conclusion from these experiments is that Ca2+ does not act as a second messenger for RVD in the Ehrlich cell.
悬浮于低渗溶液中的艾氏腹水癌细胞最初会膨胀，然后再收缩至正常体积，这一过程称为调节性容积减小（RVD）。RVD的特征是特异性地丢失氯化钾，尽管其机制目前尚不清楚。有人提出假说，即细胞内钙浓度（[Ca2+]i）升高会激活钙敏感离子通道，从而引发RVD。本研究对这一假说进行了探究。结果表明，当细胞外渗透压从300 mosM降至180 mosM时，艾氏细胞内的[Ca2+]i并未升高。RVD对钙敏感钾通道阻滞剂卡律蝎毒素（CTX）和硝苯地平不敏感，这证实了上述发现。相反，离子载体离子霉素诱导的细胞收缩对CTX和硝苯地平敏感，这表明[Ca2+]i升高可能在细胞容积减小中起作用，但这一作用是通过与RVD中观察到的机制不同的机制发生的。这些实验得出的结论是，在艾氏细胞中，Ca2+并非RVD的第二信使。
