Enhanced platelet sensitivity to prostacyclin after isosorbide-5-mononitrate in patients with stable angina pectoris.
Recently the possibility that nitrates inhibit platelet function in man has been explored in vitro and in vivo. We have studied the effect of isosorbide-5-mononitrate (ISMN), a stable and long-acting organic nitrate, on platelet function in vivo. Given orally within the current therapeutic range, the drug has practically no effect on platelet aggregation nor thromboxane generation in platelet-rich plasma in response to ADP, collagen, arachidonate, epinephrine and PAF. Synergistic effects of prostacyclin and ISMN on inhibition of ADP-induced platelet aggregation have been observed. Thus, local inhibition of platelet aggregation might not have been detectable, due to the short half-life in vitro of prostacyclin.
D000328:Adult; D000787:Angina Pectoris / Q000097:blood / Q000188:drug therapy*; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D011464:Epoprostenol / Q000494:pharmacology; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D007548:Isosorbide Dinitrate / Q000009:adverse effects / Q000031:analogs & derivatives*; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects; D013929:Thromboxane B2 / Q000097:blood
D013929:Thromboxane B2; D011464:Epoprostenol; D007548:Isosorbide Dinitrate; C030397:isosorbide-5-mononitrate