Oberleithner H, Callies C, Kusche-Vihrog K, Schillers H, Shahin V, Riethmüller C, Macgregor G A, de Wardener H E
Institute of Physiology II, University of Münster, D-48149 Münster, Germany.
Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2829-34. doi: 10.1073/pnas.0813069106. Epub 2009 Feb 6.
In the presence of aldosterone, plasma sodium in the high physiological range stiffens endothelial cells and reduces the release of nitric oxide. We now demonstrate effects of extracellular potassium on stiffness of individual cultured bovine aortic endothelial cells by using the tip of an atomic force microscope as a mechanical nanosensor. An acute increase of potassium in the physiological range swells and softens the endothelial cell and increases the release of nitric oxide. A high physiological sodium concentration, in the presence of aldosterone, prevents these changes. We propose that the potassium effects are caused by submembranous cortical fluidization because cortical actin depolymerization induced by cytochalasin D mimics the effect of high potassium. In contrast, a low dose of trypsin, known to activate sodium influx through epithelial sodium channels, stiffens the submembranous cell cortex. Obviously, the cortical actin cytoskeleton switches from gelation to solation depending on the ambient sodium and potassium concentrations, whereas the center of the cell is not involved. Such a mechanism would control endothelial deformability and nitric oxide release, and thus influence systemic blood pressure.
在醛固酮存在的情况下，处于高生理范围的血浆钠会使内皮细胞变硬，并减少一氧化氮的释放。我们现在通过使用原子力显微镜的尖端作为机械纳米传感器，来证明细胞外钾对单个培养的牛主动脉内皮细胞硬度的影响。生理范围内钾的急性增加会使内皮细胞肿胀并变软，并增加一氧化氮的释放。在醛固酮存在的情况下，高生理钠浓度会阻止这些变化。我们认为钾的作用是由膜下皮质流化引起的，因为细胞松弛素D诱导的皮质肌动蛋白解聚模拟了高钾的作用。相反，已知低剂量的胰蛋白酶可通过上皮钠通道激活钠内流，会使膜下细胞皮质变硬。显然，皮质肌动蛋白细胞骨架会根据周围钠和钾的浓度从凝胶状态转变为溶胶状态，而细胞中心则不参与其中。这样一种机制将控制内皮细胞的可变形性和一氧化氮的释放，从而影响全身血压。
