Procoagulant albumin increases vascular endothelial cell prostacyclin secretion

• Published in: Thrombosis and haemostasis Vol. 74; no. 6; p. 1573
• Main Authors: Gubler, D B, Ahlstrom, C R, Liu, L, Zhou, J F, Parker, C J, Rodgers, G M
• Format: Journal Article
• Language: English
• Published: Germany 01.12.1995
• Subjects: Aspirin - pharmacology; Binding Sites; Blood Coagulation Factors - drug effects; Blood Coagulation Factors - pharmacology; Blood Platelets - drug effects; Endothelium, Vascular - cytology; Endothelium, Vascular - drug effects; Endothelium, Vascular - secretion; Epoprostenol - secretion; Humans; Nitric Oxide - physiology; Platelet Aggregation Inhibitors - pharmacology; Prostaglandin-Endoperoxide Synthases - metabolism; Serum Albumin - drug effects; Serum Albumin - pharmacology; Suramin - pharmacology; Thromboplastin - biosynthesis; von Willebrand Factor - secretion
• ISSN: 0340-6245
• DOI: 10.1055/s-0038-1649984

Vascular endothelium regulates multiple aspects of platelet function through secretion of a variety of substances, including von Willebrand factor, nitric oxide, and prostacyclin (PGI2). The objective of this study was to determine whether procoagulant albumin (P-A1), a modified form of albumin present in normal human plasma could modulate endothelial cell secretion of these substances. P-A1 did not affect constitutive secretion of von Willebrand factor or nitric oxide, but did increase PGI2 secretion in a time- and concentration-dependent manner. Pre-treatment of endothelial cells with aspirin, or use of suramin, a broad-specificity inhibitor, prevented the response to P-A1. Prostaglandin H synthase-2 contributed to the P-A1-induced PGI2 secretion. These results indicate that in addition to inducing tissue factor activity and reducing protein C activation and fibrinolysis, P-A1 also modulates vascular endothelial cell PGI2 secretion, and potentially, platelet function.