Ziegelstein R C, Cheng L, Capogrossi M C
Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224.
Science. 1992 Oct 23;258(5082):656-9. doi: 10.1126/science.1329207.
Hemodynamic shear stress affects endothelial cell structure and function, but little is known about the signal transduction mechanisms involved in these processes. The effect of laminar shear stress on cytosolic pH (pHi) was examined in rat aortic endothelial cells cultured in glass capillary tubes. Shear stress forces led to a rapid decrease in pHi (maximal effect 0.09 pH unit at 13.4 dynes per square centimeter). Removal of specific ions or addition of exchange inhibitors suggests that in vascular endothelial cells shear stress forces activate both an alkali extruder, sodium ion-independent chloride-bicarbonate ion exchange, and an acid extruder, sodium-hydrogen ion exchange; the net effect in physiologic buffer with the bicarbonate ion is a decrease in pHi.
血流动力学切应力影响内皮细胞的结构和功能，但对于这些过程中涉及的信号转导机制却知之甚少。在玻璃毛细管中培养的大鼠主动脉内皮细胞中，研究了层流切应力对胞质pH值（pHi）的影响。切应力导致pHi迅速下降（在每平方厘米13.4达因时最大效应为0.09个pH单位）。去除特定离子或添加交换抑制剂表明，在血管内皮细胞中，切应力激活了一种碱排出体（不依赖钠离子的氯-碳酸氢根离子交换）和一种酸排出体（钠-氢离子交换）；在含有碳酸氢根离子的生理缓冲液中的净效应是pHi降低。
