Nitric oxide modulates endothelin 1-induced Ca2+ mobilization and cytoskeletal F-actin filaments in human cerebromicrovascular endothelial cells

Ye Chen, Richard M. McCarron, Joliet Bembry, Christi Ruetzler, Nabil Azzam, Fred A. Lenz, Maria Spatz

Research output: Contribution to journalArticle


A functional interrelation between nitric oxide (NO), the endothelial- derived vasodilating factor, and endothelin 1 (ET-1), the potent vasoconstrictive peptide, was investigated in microvascular endothelium of human brain. Nor-1 dose-dependently decreased the ET-1-stimulated mobilization of Ca2+. This response was mimicked with cGMP and abrogated by inhibitors of guanylyl cyclase or cGMP-dependent protein kinase G. These findings indicate that NO and ET-1 interactions involved in modulation of intracellular Ca2+ are mediated by cGMP/protein kinase G. In addition, Nor- 1-mediated effects were associated with rearrangements of cytoskeleton F- actin filaments. The results suggest mechanisms by which NO-ET-1 interactions may contribute to regulation of microvascular function.

Original languageEnglish (US)
Pages (from-to)133-138
Number of pages6
JournalJournal of Cerebral Blood Flow and Metabolism
Issue number2
StatePublished - Jan 1 1999



  • Actin
  • Brain endothelial cells
  • Ca Mobilization
  • Nitric oxide
  • cGMP Endothelin

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine

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