Potassium softens vascular endothelium and increases nitric oxide release

H. Oberleithner*, C. Callies, K. Kusche-Vihrog, H. Schillers, V. Shahin, C. Riethmuller, G. A. MacGregor, H. E. De Wardener

*Corresponding author for this work
132 Citations (Scopus)


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.

Original languageEnglish
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number8
Pages (from-to)2829-2834
Number of pages6
Publication statusPublished - 24.02.2009

Research Areas and Centers

  • Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)


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