Activation of endothelial guanylate cyclase inhibits cellular reactivity

R. Heller, F. Bussolino, D. Ghigo, G. P. Pescarmona, R. Calvino, A. Gasco, U. Till, A. Bosia

Research output: Contribution to journalArticlepeer-review


The study shows that endothelial cells from human umbilical veins have a soluble guanylate cyclase which can be activated by sodium nitroprusside (SNP), SIN-1 (3-morpholinosydnonimine) and S35b (4-methyl-3-phenylsulfonylfuroxan). Cells which were pretreated with these compounds showed an inhibition of thrombin-induced arachidonic acid release, PGI 2 formation, PAF synthesis and PMNL adhesion. Endothelial guanylate cyclase can also be activated by nitric oxide (NO) which is generated in endothelial cells upon stimulation with thrombin or ionomycin. It is suggested that endogenously produced NO might control cell activation and endothelial function through a cGMP-dependent mechanism.

Original languageEnglish
Pages (from-to)177-181
Number of pages5
JournalAgents and Actions
Issue numberSUPPL. I
Publication statusPublished - 1995

ASJC Scopus subject areas

  • Pharmacology (medical)
  • Toxicology


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