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Endothelial cell swelling by aldosterone.

H Oberleithner1, S W Schneider, L Albermann

  • 1Institute of Physiology I, Nanolab, University of Münster, Robert-Koch-Str. 27a, D-48149 Münster, Germany. oberlei@uni-muenster.de

The Journal of Membrane Biology
|January 16, 2004
PubMed
Summary
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Aldosterone rapidly increases human endothelial cell volume, with later effects blocked by spironolactone or amiloride, suggesting therapeutic potential for aldosterone-induced vascular issues.

Area of Science:

  • Cardiovascular Biology
  • Endocrinology
  • Cell Physiology

Background:

  • Mineralocorticoids, like aldosterone, impact the cardiovascular system beyond the kidneys.
  • Understanding aldosterone's cellular effects is crucial for treating cardiovascular diseases.

Purpose of the Study:

  • To investigate the immediate and short-term effects of aldosterone on human umbilical venous endothelial cells (HUVECs).
  • To determine the role of mineralocorticoid receptors and ion transport in aldosterone-induced cellular changes.

Main Methods:

  • Human umbilical venous endothelial cells (HUVECs) were treated with aldosterone.
  • Atomic force microscopy (AFM) was used to measure cell and nuclear volume dynamics.
  • The effects of aldosterone antagonist spironolactone and transport inhibitors (amiloride, cariporide) were assessed.

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Main Results:

  • Aldosterone caused an immediate (1 min) cell swelling (10%), followed by maximal swelling (18%) at 10 min.
  • Spironolactone and amiloride blocked the late swelling but not the initial response.
  • Aldosterone induced transient nuclear swelling followed by shrinkage; cariporide had no effect.

Conclusions:

  • Aldosterone triggers rapid swelling independent of mineralocorticoid receptors and Na+ channels, followed by receptor- and channel-dependent late swelling.
  • Intracellular shifts of macromolecules underlie aldosterone-induced cell volume changes.
  • Amiloride and spironolactone show potential for preventing aldosterone-induced vasculopathies.