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Furosemide in vitro is an inhibitor of primary ADP-induced platelet aggregation. As such, furosemide also inhibits collagen-induced aggregation and the secondary wave of epinephrine-induced aggregation. Concentrations of furosemide which clearly inhibit collagen-induced platelet aggregation do not inhibit collagen-induced release of ADP. Thus the effect of furosemide is distinct from that of aspirin and other anti-inflammatory drugs which inhibit platelet release but do not inhibit primary ADP-induced platelet aggregation. The inhibitory effect of furosemide is competitive, demonstrable in heparinized as well as citrated platelet-rich plasma, and it is not corrected by calcium. The concentration of furosemide required for in vitro inhibition (1 to 5mM) can not be achieved in vivo. However, the study of compounds related to furosemide could lead to the discovery of a clinically useful inhibitor of primary ADP-induced platelet aggregation.
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Accepted: September 29, 1972
Received: March 28, 1972
☆This work was supported by the Paul V. Galvin Charitable Trust.
© 1973 Published by Elsevier Inc.