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Related Experiment Video

Updated: Jun 25, 2026

Isolation and Adoptive Transfer of High Salt Treated Antigen-presenting Dendritic Cells

Isolation and Adoptive Transfer of High Salt Treated Antigen-presenting Dendritic Cells

Published on: March 5, 2019

Aldosterone activates endothelial exocytosis.

Youngtae Jeong¹, Damian F Chaupin, Kenji Matsushita

¹Department of Medicine, Graduate Program in Pathobiology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

Proceedings of the National Academy of Sciences of the United States of America

|February 19, 2009

Summary

Aldosterone triggers vascular inflammation by initiating endothelial cell exocytosis, a rapid, nongenomic process mediated by the mineralocorticoid receptor (MR). Blocking the MR may reduce inflammation and cardiac fibrosis.

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Published on: September 26, 2018

Area of Science:

Cardiovascular Biology
Endothelial Cell Biology
Inflammation Research

Background:

Elevated aldosterone levels are linked to vascular inflammation, but the underlying proinflammatory pathways remain unclear.
Understanding aldosterone's role in endothelial cell function is crucial for developing targeted therapies.

Purpose of the Study:

To elucidate the molecular mechanisms by which aldosterone contributes to vascular inflammation.
To investigate the role of the mineralocorticoid receptor (MR) in aldosterone-induced endothelial responses.

Main Methods:

Assessed aldosterone-induced endothelial cell exocytosis of Weibel-Palade bodies.
Evaluated the effects of spironolactone (MR blocker) and MR knockdown on exocytosis.
Determined the genomic or nongenomic nature of aldosterone's effect using actinomycin D.
Measured leukocyte adherence to endothelial cells following aldosterone treatment.

Main Results:

Aldosterone stimulates endothelial exocytosis, externalizing P-selectin and releasing von Willebrand factor.
Spironolactone and MR knockdown antagonize aldosterone-induced exocytosis, confirming MR mediation.
Aldosterone's effect on exocytosis is rapid and not inhibited by actinomycin D, indicating a nongenomic pathway.
Aldosterone treatment increases leukocyte adherence to endothelial cells.

Conclusions:

Aldosterone activates vascular inflammation partly via nongenomic, MR-mediated pathways involving endothelial exocytosis.
Aldosterone antagonism may mitigate vascular inflammation and cardiac fibrosis by inhibiting endothelial exocytosis.