Thromb Haemost 2002; 88(06): 1060-1065
DOI: 10.1055/s-0037-1613355
Involvement of Thrombin Receptors in the Subject-dependent Variability in Ca2+ Signal Generation
Schattauer GmbH

Regulation by Nitric Oxide of Endotoxin-Induced Tissue Factor and Plasminogen Activator Inhibitor-1 in Endothelial Cells

Ana Pérez-Ruiz
1   Haemostasis and Thrombosis Research Unit, School of Medicine, University of Navarra, Pamplona
,
Ramón Montes
1   Haemostasis and Thrombosis Research Unit, School of Medicine, University of Navarra, Pamplona
,
Francisco Velasco
2   Department of Research, Reina Sofía University Hopsital, Cordoba
,
Chary López-Pedrera
2   Department of Research, Reina Sofía University Hopsital, Cordoba
,
José Antonio Páramo
3   Haematology Service, University Clinic, School of Medicine, University of Navarra, Pamplona
4   Atherosclerosis Research Unit, School of Medicine, University of Navarra, Pamplona, Spain
,
Josune Orbe
4   Atherosclerosis Research Unit, School of Medicine, University of Navarra, Pamplona, Spain
,
José Hermida
1   Haemostasis and Thrombosis Research Unit, School of Medicine, University of Navarra, Pamplona
3   Haematology Service, University Clinic, School of Medicine, University of Navarra, Pamplona
,
Eduardo Rocha
1   Haemostasis and Thrombosis Research Unit, School of Medicine, University of Navarra, Pamplona
3   Haematology Service, University Clinic, School of Medicine, University of Navarra, Pamplona
› Author Affiliations
Further Information

Publication History

Received 04 March 2002

Accepted 16 September 2002

Publication Date:
09 December 2017 (online)

Summary

The increase in nitric oxide (NO) production in lipopolysaccharide (LPS)-induced sepsis is thought to contribute to the development of shock. However, NO could also play an antithrombotic role. Little is known about the modulating effect of NO on the endothelial overexpression and production of tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) occurring in endotoxemia. We analyzed the effect of N(G)-nitro-L-arginine-methyl-ester (L-NAME), an inhibitor of NO synthases, and S-nitroso-N-acetyl-D,L-penicillamine (SNAP), a NO donor, on the expression and synthesis of TF and PAI-1 by LPS-challenged human umbilical vein endothelial cells (HUVEC): L-NAME enhanced the increase in TF mRNA and antigen levels (P <0.05) observed in LPS-treated HUVEC; SNAP down-regulated the LPSinduced TF increment (p <0.05). However, no effects of NO on regulation of the LPS-dependent increase in PAI-1 could be seen. Thus, NO could play an antithrombotic role in sepsis by down-regulating the endothelial overexpression and production of TF.

 
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