Potassium softens vascular endothelium and increases nitric oxide release

Area of Science:

• Cardiovascular Physiology
• Cell Biology
• Biophysics

Background:

• Aldosterone and high plasma sodium stiffen endothelial cells, reducing nitric oxide (NO).
• The role of extracellular potassium in endothelial cell mechanics and NO release is less understood.

Purpose of the Study:

• To investigate the effects of extracellular potassium on the mechanical properties of individual endothelial cells.
• To determine how potassium influences nitric oxide release in the context of sodium and aldosterone levels.

Main Methods:

• Utilized atomic force microscopy (AFM) with a mechanical nanosensor to measure the stiffness of cultured bovine aortic endothelial cells.
• Manipulated extracellular potassium and sodium concentrations, and aldosterone levels.
• Assessed nitric oxide release and cell volume changes.

Main Results:

• Acute increases in physiological extracellular potassium swelled and softened endothelial cells.
• Elevated potassium significantly increased nitric oxide release.
• High physiological sodium, in the presence of aldosterone, counteracted the softening and NO-increasing effects of potassium.
• Cytochalasin D mimicked high potassium's effects, suggesting actin depolymerization.
• Trypsin, activating sodium influx, stiffened the cell cortex.

Conclusions:

• Extracellular potassium concentration directly modulates endothelial cell stiffness and nitric oxide release.
• The submembranous cortical actin cytoskeleton's state (gelation/solation) is sensitive to ambient sodium and potassium levels.
• This potassium-mediated mechanism controlling endothelial deformability and NO release may influence systemic blood pressure.