Organic nitrates, cornerstones of antianginal therapy, are believed to exert their principal anti-ischemic benefit by relaxing vascular smooth muscle. Recent evidence suggests that these compounds and related nitro(so) vasodilators are also potent platelet inhibitors. In view of the well recognized role of thrombotic events mediated by platelets in acute coronary syndromes, the antiplatelet effect of nitrates may also be of mechanistic importance in the treatment of these disorders. This review details the biochemical mechanism by which nitro(so) compounds inhibit platelet function and summarizes the in vitro and in vivo evidence that supports their antithrombotic effects.