Abstract
Platelets are important constituents of hemostasis under normal and pathophysiological circumstances (Marcus and Safier 1993). Following injury, platelet aggregation helps prevent excessive blood loss and also plays an essential role in atherosclerosis and thrombosis, where it is implicated in the pathogenesis of life-threatening diseases, e.g., myocardial infarction and stroke. The hallmark of platelet function is aggregation that is regulated by an array of activating and inhibiting hormones and factors released by surrounding cells or from platelets themselves. Activators of platelets include enzymes such as the protease thrombin, lipid mediators such as platelet activating factor (PAF) and thromboxane A2 (TXA2), nucleotides (ADP), and various neurotransmitters, e.g., catecholamines (via (α 2-adrenoceptors) and serotonin. In contrast, platelet aggregation is inhibited by adenosine, prostaglandins, e.g., prostacyclin (PGI2), or catecholamines (via β-adrenoceptors). All these ligands bind to cell surface receptors exhibiting a high degree of structural homology regardless of whether or not these receptors elicit stimulating or inhibiting signals (Hourani and Cusack 1991).
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Koesling, D., Nürnberg, B. (1997). Platelet G Proteins and Adenylyl and Guanylyl Cyclases. In: von Bruchhausen, F., Walter, U. (eds) Platelets and Their Factors. Handbook of Experimental Pharmacology, vol 126. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60639-7_9
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