Pierce S K, Politis A D, Smith L H, Rowland L M
Department of Zoology, University of Maryland, Baltimore.
Cell Calcium. 1988 Jun;9(3):129-40. doi: 10.1016/0143-4160(88)90016-4.
The phenomenon of cell volume recovery following a hypo-osmotic stress mediated by intracellular osmolyte regulation is well known. In many, perhaps all, cell types, the osmolytes involved are usually inorganic ions and amino acids. The details of the regulatory mechanisms for the organic-type osmolytes are not well known. We have found that an immediate influx of external Ca2+ occurs coincident with the application of a hypo-osmotic stress into red cells of two invertebrate species. In both, the influx is initiated by the osmotic stress, not the concomitant ionic decrease. Volume recovery in clam red blood cells is blocked by phenothiazines. In addition, the effect of the phenothiazines is to reduce the amino acid efflux; the ionic portion of the volume response is unaffected. In contrast, the phenothiazines potentiate the volume recovery in worm red coelomocytes. A23187 also potentiates the volume recovery of the worm red cells. The results suggest that the Ca2+ influx is involved in the mechanism that alters cell membrane permeability permitting the amino acid efflux by a mechanism that may involve calmodulin.
由细胞内渗透溶质调节介导的低渗应激后细胞体积恢复现象是众所周知的。在许多（或许所有）细胞类型中，所涉及的渗透溶质通常是无机离子和氨基酸。有机型渗透溶质的调节机制细节尚不清楚。我们发现，在对两种无脊椎动物的红细胞施加低渗应激时，会同时出现外部Ca2+的立即流入。在这两种动物中，流入是由渗透应激引发的，而非伴随的离子减少。吩噻嗪可阻断蛤红细胞的体积恢复。此外，吩噻嗪的作用是减少氨基酸外流；体积反应的离子部分不受影响。相比之下，吩噻嗪可增强蠕虫红色体腔细胞的体积恢复。A23187也可增强蠕虫红细胞的体积恢复。结果表明，Ca2+流入参与了改变细胞膜通透性的机制，该机制可能通过涉及钙调蛋白的方式允许氨基酸外流。
