title: Potassium softens vascular endothelium and increases nitric oxide release.
abstract: 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.
authors.affiliation: Institute of Physiology II, University of Münster, D-48149 Münster, Germany. oberlei@uni-muenster.de
authors.forename: H
authors.initials: H
authors.lastname: Oberleithner
authors.forename: C
authors.initials: C
authors.lastname: Callies
authors.forename: K
authors.initials: K
authors.lastname: Kusche-Vihrog
authors.forename: H
authors.initials: H
authors.lastname: Schillers
authors.forename: V
authors.initials: V
authors.lastname: Shahin
authors.forename: C
authors.initials: C
authors.lastname: Riethmüller
authors.forename: G A
authors.initials: GA
authors.lastname: Macgregor
authors.forename: H E
authors.initials: HE
authors.lastname: de Wardener
mesh_terms: D000199:Actins / Q000378:metabolism; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D002417:Cattle; D015638:Cytochalasin D / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism; D053503:Epithelial Sodium Channels / Q000187:drug effects / Q000378:metabolism; D018625:Microscopy, Atomic Force; D009569:Nitric Oxide / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology*; D014357:Trypsin / Q000494:pharmacology
chemical_list: D000199:Actins; D053503:Epithelial Sodium Channels; D015638:Cytochalasin D; D009569:Nitric Oxide; D000584:Amiloride; D014357:Trypsin; D011188:Potassium