By A. G. Herman (auth.), Arnold G. Herman (eds.)
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Extra info for Antithrombotics: Pathophysiological Rationale for Pharmacological Interventions
137. , Swies, J. (1985) The influence of molsidomine and its active metabolite SIN-Ion fibrinolysis and platelet aggregation. Thromb. Haemost. 54,746-749. 138. , Weichert, W. (1987) Inhibition of platelet thrombus formation in rat mesenteric vessels by molsidomine and SIN-I. Path. BioI. 35,223-225 (in French). 139. E. (1987) Inhibition of platelet function in animals by molsidomine. Path. BioI. 35,226-228 (in French) . 140. Reden, J. (1990) Molsidomine. Blood Vessels 27,282-294. 141. , Soria, C.
Chem. 263, 1982719832. 26. J. , BUNTING, S. A. (1990) 'Platelet glycoprotein lIb-IlIa protein antagonists from snake venoms. Evidence for a family of platelet-aggregation inhibitors', Proc. Natl. Acad. Sci. USA. 87, 2471-2475. 27. R. E. (1987) 'Abolition of in vivo platelet thrombus formation with monoclonal antibodies to the platelet GPllb/llla receptor : correlation with platelet aggregation and bleeding time', Thromb. Haemostasis 58, 244. 28. A. D. (1985) 'Effect of platelet-modifying drugs on arterial thromboembolism in baboons : aspirin potentiates the antithrombotic actions of dipyridamole and sulfinpyrazone by mechanism(s) independent of platelet cyclooxygenase inhibition' J.
The subsequent biochemical effects triggered by this nucleotide in platelets may result in: inhibition of phosphorylation of myosin light chains and of protein kinase C stimulation of phosphorylation of the betasubunit of glycoprotein I, and modulation of phospholipase A2- and C- mediated responses [28-35). Stimulation of NO release in cultured endothelium results in activation of SGC activity and elevation of cyclic GMP levels in the endothelium itself [36-38). Cyclic GMP causes 0 0 - - ROLE OF NITRIC OXIDE IN ENDOTHELIAL CELL-PLATELET INTERACTIONS 29 inhibition of inositol 1,4,5- triphosphate formation, probably by a G protein - mediated mechanism .