Cheung R K, Grinstein S, Dosch H M, Gelfand E W
J Cell Physiol. 1982 Aug;112(2):189-96. doi: 10.1002/jcp.1041120206.
The mechanism of volume regulation in hypotonic media was analysed in human peripheral blood mononuclear (PBM) cells. Electronic cell sizing showed that hypotonic swelling is followed by a regulatory volume decrease (RVD) phase. This was confirmed by both electron microscopy and by cellular water determinations. The rate of regulatory shrinking was proportional to the degree of hypotonicity in the 0.5-0.9 X isotonic range. Cell viability was only marginally affected in this range. The content of cellular K+ decreased during RVD, while Na+ content remained unchanged. Similarly, the efflux of 86Rb (used as a K+ analog) increased upon dilution, whereas 22Na efflux was not altered. 86Rb uptake was enhanced by hypotonic stress and both ouabain-sensitive and -insensitive components were affected. A ouabain-sensitive stimulation was also seen in Na+- free media. Ouabain partially inhibited RVD only if added to the cells hours before hypotonic challenge. A normal shrinking response was observed in K+-free media, and also in Na+-free media when Li+, choline+, or Tris+ were the substitutes. In high K+ or RB+ hypotonic media shrinking was absent and a second swelling phase was observed. Cs+ displayed an intermediate behavior, with shrinking observed at lower dilutions and secondary swelling at higher ones. The direction and magnitude of the response also changed when the external K+ concentration was varied and, with 50 mM K+, no regulatory volume change occurred following hypotonic stress. These findings suggest that RVD occurs largely by a passive loss of cellular K+, resulting from a selective increase in permeability to this ion. In addition, the (Na-K) pump appears to be activated upon cell swelling by a mechanism other than Na+ entry into the cell, but this activation is not essential for RVD.
对人外周血单核（PBM）细胞在低渗介质中的体积调节机制进行了分析。电子细胞大小测定显示，低渗肿胀之后是调节性体积减小（RVD）阶段。这通过电子显微镜和细胞含水量测定得到了证实。在0.5 - 0.9倍等渗范围内，调节性收缩速率与低渗程度成正比。在此范围内细胞活力仅受到轻微影响。在RVD期间，细胞内K⁺含量降低，而Na⁺含量保持不变。同样，稀释后⁸⁶Rb（用作K⁺类似物）的外流增加，而²²Na外流未改变。低渗应激增强了⁸⁶Rb的摄取，哇巴因敏感和不敏感成分均受到影响。在无Na⁺介质中也观察到哇巴因敏感的刺激作用。仅在低渗刺激前数小时将哇巴因添加到细胞中时，它才会部分抑制RVD。在无K⁺介质中观察到正常的收缩反应，当Li⁺、胆碱⁺或Tris⁺作为替代物时，在无Na⁺介质中也观察到正常收缩反应。在高K⁺或RB⁺低渗介质中没有收缩现象，而是观察到第二个肿胀阶段。Cs⁺表现出中间行为，在较低稀释度下观察到收缩，在较高稀释度下观察到二次肿胀。当外部K⁺浓度变化时，反应的方向和幅度也会改变，当K⁺浓度为50 mM时，低渗应激后未发生调节性体积变化。这些发现表明，RVD主要是由于细胞对K⁺的通透性选择性增加导致细胞内K⁺被动丢失而发生的。此外，（Na - K）泵似乎在细胞肿胀时通过Na⁺进入细胞以外的机制被激活，但这种激活对于RVD并非必不可少。
