N-acetylcysteine potentiates platelet inhibition by endothelium-derived relaxing factor.

Journal Article

Recent evidence suggests that endothelium-derived relaxing factor exhibits properties of nitric oxide. Like nitric oxide, it inhibits platelet function and mediates its effects by elevating intracellular cyclic GMP. In this study we have investigated the role of reduced thiol in the mechanism of action of endothelium-derived relaxing factor on platelets. Bovine aortic endothelial cells were grown on microcarrier beads and pretreated with aspirin before use. Endothelial cells stimulated with bradykinin or exposed to stirred medium expressed a dose-dependent inhibition of platelet aggregation that was potentiated by the reduced thiol, N-acetylcysteine. Endothelial cell-mediated platelet inhibition was attenuated by methylene blue. Inhibition of platelet aggregation by endothelial cells was associated with a rise in platelet intracellular cyclic GMP, an effect that was enhanced by N-acetylcysteine. These data show that 1) the reduced thiol N-acetylcysteine potentiates platelet inhibition by endothelium-derived relaxing factor and 2) this effect is associated with increasing intracellular platelet cyclic GMP levels.

Full Text

Duke Authors

Cited Authors

  • Stamler, J; Mendelsohn, ME; Amarante, P; Smick, D; Andon, N; Davies, PF; Cooke, JP; Loscalzo, J

Published Date

  • September 1989

Published In

Volume / Issue

  • 65 / 3

Start / End Page

  • 789 - 795

PubMed ID

  • 2548765

Pubmed Central ID

  • 2548765

International Standard Serial Number (ISSN)

  • 0009-7330

Digital Object Identifier (DOI)

  • 10.1161/01.res.65.3.789


  • eng

Conference Location

  • United States