The role of nitric oxide and cGMP in platelet adhesion to vascular endothelium

• Published in: Biochemical and biophysical research communications Vol. 148; no. 3; pp. 1482 - 1489
• Main Authors: Radomski, Marek W., Palmer, Richard M.J., Moncada, Salvador
• Format: Journal Article
• Language: English
• Published: San Diego, CA Elsevier Inc 13.11.1987; Elsevier
• Subjects: 3',5'-Cyclic-GMP Phosphodiesterases - antagonists & inhibitors; Applied sciences; Aspirin - pharmacology; Blood Platelets - physiology; Collagen - physiology; Cyclic GMP - pharmacology; Endothelium, Vascular - physiology; Epoprostenol - pharmacology; Exact sciences and technology; Extracellular Matrix - physiology; Humans; In Vitro Techniques; Nitric Oxide - pharmacology; Other techniques and industries; Phthalazines - pharmacology; Platelet Adhesiveness - drug effects; Purinones - pharmacology; Superoxide Dismutase - metabolism; Thrombin - metabolism
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/S0006-291X(87)80299-1

The inhibition of platelet adhesion by nitric oxide (NO) and prostacyclin and their mechanism of action was studied. Platelet adhesion to collagen fibrils and endothelial cell matrix was inhibited completely by NO but only partially by prostacyclin. Adhesion of platelets to endothelial cell monolayers was inhibited by bradykinin. This effect of bradykinin was unaffected by aspirin, and was accounted for by the amounts of NO released by the endothelial cells. Inhibition of platelet adhesion by NO and prostacyclin was potentiated by selective inhibitors of cGMP phosphodiesterase, but not of cAMP phosphodiesterase, indicating that elevation of cGMP regulates platelet adhesion.