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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:158.)
© 2003 American Heart Association, Inc.

Editorials

Advantages of Fast-Acting ADP Receptor Blockade in Ischemic Heart Disease

Alan T. Nurden; Paquita Nurden

From the UMR 5533 CNRS, Hôpital Cardiologique, Pessac, France.

Correspondence to Dr Alan T. Nurden, UMR 5533 CNRS, Hôpital Cardiologique, 33604 Pessac, France. E-mail Alan.Nurden@cnrshl.u-bordeaux2.fr

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The stimulatory role of ADP in platelet aggregation has received much attention in recent years.¹ Not only is ADP a major physiological agonist on its own, it also plays a key role in promoting aggregation by other stimuli of which collagen and epinephrine are excellent examples. Released from damaged tissues and blood cells, including secreting platelets, ADP is a major factor in coronary artery disease favoring platelet accumulation at sites of stenosis and fissured atherosclerotic plaques. Recent advances have defined how ADP activates platelets in a process involving two receptors, P2Y₁ and P2Y₁₂, both belonging to the G-protein–coupled seven-transmembrane domain receptor family. Studies were advanced by the discovery of patients in which P2Y₁₂ is congenitally deficient^2,3 and by the recent cloning of P2Y₁₂ which had proved a most elusive receptor.^2–5 According to current thinking, interaction of platelets with P2Y₁ leads to shape change, calcium mobilization, and a rapidly reversible aggregation. Simultaneous binding to P2Y₁₂ permits the formation of large, stable platelet aggregates. It appears that P2Y₁ starts the aggregation, and then P2Y₁₂ takes over. This role of P2Y₁₂ had been speculated on before its cloning when, as the mysterious "P_2T," it was already considered to be a primary target for antithrombotic therapy. It has now been confirmed that P2Y₁₂ is the site of action of the long-acting antithrombotic drugs clopidogrel and ticlopidine, widely used to downregulate platelet reactivity in coronary artery disease.⁶ A third purported platelet receptor for ADP, the ion channel P2X₁, is now known to . . . [Full Text of this Article]

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