Potassium softens vascular endothelium and increases nitric oxide release

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 fo...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2009-02, Vol.106 (8), p.2829-2834
Main Authors: Oberleithner, H, Callies, C, Kusche-Vihrog, K, Schillers, H, Shahin, V, Riethmüller, C, MacGregor, G.A, de Wardener, H.E
Format: Article
Language:English
Subjects:
Actins
Actins - metabolism
Amiloride - pharmacology
Animals
Biological Sciences
Cattle
Cell culture
Cell membranes
Cultured cells
Cytochalasin D - pharmacology
Effects
Endothelial cells
Endothelium
Endothelium, Vascular - drug effects
Endothelium, Vascular - metabolism
Epithelial Sodium Channels - drug effects
Epithelial Sodium Channels - metabolism
Hormones
Microscopy, Atomic Force
Nitric oxide
Nitric Oxide - metabolism
Nitrites
Oxides
Potassium
Potassium - pharmacology
Sodium
Stiffness
Trypsin - pharmacology
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Summary: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.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.0813069106