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• W2019964097 abstract "Organic nitrates are believed to provide relief from angina principally by dilating the coronary vasculature. Substantial evidence exists, however, to support a potent antiplatelet effect for these agents as well. Each of these compounds ultimately is metabolized to nitric oxide (or an S-nitrosothiol congener thereof), and this metabolite, in turn, is a potent activator of platelet guanylate cyclase. Activation of guanylate cyclase increases platelet cyclic guanosine monophosphate (cGMP), and is accompanied by inhibition of agonist-mediated calcium flux, and, in turn, reduction of fibrinogen binding to the glycoprotein IIb/IIIa receptor. Since fibrinogen binding is essential for platelet aggregation regardless of the agonist involved, its inhibition appears to be the critical mechanism by which platelet function is impaired by these agents. The recently recognized role that platelet-dependent thrombotic processes play in acute coronary syndromes suggests that the inhibition of platelets by nitrates may offer an additional mechanism by which these compounds improve perfusion to ischemic myocardium." @default.
• W2019964097 created "2016-06-24" @default.
• W2019964097 creator A5028396638 @default.
• W2019964097 date "1992-09-01" @default.
• W2019964097 modified "2023-10-18" @default.
• W2019964097 title "Antiplatelet and antithrombotic effects of organic nitrates" @default.
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• W2019964097 doi "https://doi.org/10.1016/0002-9149(92)90590-u" @default.
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