The long-term exposure of endothelial cells to molsidomine increases their antithrombogenicity by inducing the production of nitric oxide-related chemical substances

• Published in: Journal of cardiovascular pharmacology Vol. 14 Suppl 11; p. S98
• Main Authors: Berenger-Bahuet, F P, Rolland, P H
• Format: Journal Article
• Language: English
• Published: United States 1989
• Subjects: Analysis of Variance; Animals; Cells, Cultured; Endothelium, Vascular - drug effects; Endothelium, Vascular - metabolism; Femoral Artery; Molsidomine - pharmacology; Nitric Oxide - metabolism; Nitric Oxide - pharmacology; Platelet Aggregation - drug effects; Platelet Aggregation Inhibitors - pharmacology; Rodentia; Time Factors
• ISSN: 0160-2446
• DOI: 10.1097/00005344-198906152-00019

Long-term exposure of endothelial cells to molsidomine in vivo and in vitro improves the thromboresistance of endothelial cells, judging from the inhibition of platelet aggregation by endothelial cells in autologous plasma. In cultured endothelial cells, the present studies attempted (a) to show that platelets influence the release by endothelial cells of soluble factors accounting for antiplatelet activity and (b) to elucidate whether these factors may be related to nitric oxide (NO). The production of NO was quantified from the spectral conversion of oxyhemoglobin to methemoglobin and was also evaluated spectrophotometrically after diazotization of sulfanilic acid and coupling with N-(1-naphthyl)ethylenediamine. The results suggest that (a) the inhibition of platelet aggregation by endothelial cells results from antiaggregating factor(s) that are released by the cells when stimulated by platelets; and (b) NO or related chemical substances are produced by endothelial cells following long-term exposure of cells to molsidomine, whereas a basal release of NO by control cells was not detected. These findings suggest that NO accounts for the molsidomine-sensitive mechanisms of endothelial cell-mediated inhibition of platelet aggregation.