Sodium renders endothelial cells sticky for red blood cells
Sodium renders endothelial cells sticky for red blood cells
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DOI：
10.3389/fphys.2015.00188
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发表时间：
2015-06-30
影响因子：
4
通讯作者：
Kusche-Vihrog, Kristina
中科院分区：
文献类型：
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作者：
Oberleithner, Hans;Waelte, Mike;Kusche-Vihrog, Kristina
红细胞 (RBC) 和血管内皮细胞 (EC) 糖萼中的负电荷有助于血液无摩擦地流过血管。 Na+选择性地屏蔽这些控制表面电负性的电荷。解决了环境 Na+ 浓度是否控制 RBC-EC 相互作用的问题。使用原子力显微镜（AFM）对红细胞和内皮糖萼之间的粘附力进行量化。将安装在 AFM 悬臂上的单个红细胞与内皮表面进行物理接触，然后将其拉出。 (i) 酶法去除糖萼中的负电荷后，(ii) 在不同环境 Na+ 下，以及 (iii) 应用细胞内醛固酮受体拮抗剂螺内酯后，对粘附力进行量化。去除表面负电荷会增加 RBC-EC 相互作用力。环境 Na+ 从 133 mM 逐步增加到 140 mM 不会影响它们。然而，超过 140 mM Na+ 粘附力急剧增加（Na+ 每增加 1 mM，粘附力增加 10%）。螺内酯可以防止这种反应。结论是负电荷降低了 RBC 和 EC 之间的粘附力。环境 Na+ 浓度决定了自由负电荷的可用性。低生理范围（低于 140 mM）的 Na+ 浓度允许有足够量的空负电荷，因此红细胞与内皮表面的粘附较小。相比之下，高生理范围（超过 140 mM）的 Na+ 会使剩余的负表面电荷饱和，从而增加粘附力。螺内酯阻断醛固酮受体可防止 Na+ 诱导的红细胞粘附到内皮糖萼。将体外实验外推到体内条件得出这样的假设：高钠摄入量可能会增加血栓事件的发生率。
Negative charges in the glycocalyx of red blood cells (RBC) and vascular endothelial cells (EC) facilitate frictionless blood flow through blood vessels. Na+ selectively shields these charges controlling surface electronegativity. The question was addressed whether the ambient Na+ concentration controls RBC-EC interaction. Using atomic force microscopy (AFM) adhesion forces between RBC and endothelial glycocalyx were quantified. A single RBC, mounted on an AFM cantilever, was brought in physical contact with the endothelial surface and then pulled off. Adhesion forces were quantified (i) after enzymatic removal of negative charges in the glycocalyx, (ii) under different ambient Na+ and (iii) after applying the intracellular aldosterone receptor antagonist spironolactone. Removal of negative surface charges increases RBC-EC interaction forces. A stepwise increase of ambient Na+ from 133 to 140 mM does not affect them. However, beyond 140 mM Na+ adhesion forces increase sharply (10% increase of adhesion force per 1 mM increase of Na+). Spironolactone prevents this response. It is concluded that negative charges reduce adhesion between RBC and EC. Ambient Na+ concentration determines the availability of free negative charges. Na+ concentrations in the low physiological range (below 140 mM) allow sufficient amounts of vacant negative charges so that adhesion of RBC to the endothelial surface is small. In contrast, Na+ in the high physiological range (beyond 140 mM) saturates the remaining negative surface charges thus increasing adhesion. Aldosterone receptor blockade by spironolactone prevents Na+ induced RBC adhesion to the endothelial glycocalyx. Extrapolation of in vitro experiments to in vivo conditions leads to the hypothesis that high sodium intake is likely to increase the incidence of thrombotic events.