Aldosterone activates endothelial exocytosis

Youngtae Jeong, Damian F. Chaupin, Kenji Matsushita, Munekazu Yamakuchi, Scott J. Cameron, Craig N. Morrell, Charles J. Lowenstein

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


Although elevated levels of aldosterone are associated with vascular inflammation, the proinflammatory pathways of aldosterone are not completely defined. We now show that aldosterone triggers endothelial cell exocytosis, the first step in leukocyte trafficking. Exogenous aldosterone stimulates endothelial exocytosis of Weibel-Palade bodies, externalizing P-selectin and releasing von Willebrand factor. Spironolactone, a nonselective mineralocorticoid receptor (MR) blocker, antagonizes aldosterone-induced endothelial exocytosis. Knockdown of the MR also decreases exocytosis, suggesting that the MR mediates exocytosis. Aldosterone triggers exocytosis within minutes, and this effect is not inhibited by actinomycin D, suggesting a nongenomic effect of aldosterone. Aldosterone treatment of endothelial cells increases leukocyte adherence to endothelial cells in culture. Taken together, our data suggest that aldosterone activates vascular inflammation in part through nongenomic, MR-mediated pathways. Aldosterone antagonism may decrease vascular inflammation and cardiac fibrosis in part by blocking endothelial exocytosis.

Original languageEnglish (US)
Pages (from-to)3782-3787
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number10
StatePublished - Mar 10 2009


  • Inflammation
  • Mineralocorticoid
  • Nitric oxide
  • P-selectin
  • Vascular

ASJC Scopus subject areas

  • General


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