Abstract
Prostacyclin (PGI2) is a naturally occurring prostaglandin released by vascular tissues, which possesses platelet antiaggregatory and vasodilatory properties [1]. PGI2 interacts with specific receptors on platelets, and it increases intracellular cAMP levels through activation of the adenylate cyclase enzyme [2]. Platelets of patients suffering from pathological conditions associated with increased platelet aggregability displayed, in vitro, reduced sensitivity to the inhibitory effects of PGI2 [3, 4]. Previous studies by our group have shown that in patients with type Ila hypercholesterolemia, higher concentrations of PGI2 were required to inhibit the in vitro-induced platelet aggregation, in comparison with platelets from normolipidemic subjects [5]. The alterations observed in platelets from type Ila patients were not due to differences in the capability of PGI2 to stimulate platelet adenylate cyclase [5].
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References
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© 1987 Springer-Verlag, Berlin Heidelberg
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Tremoli, E., Maderna, P., Mannucci, L., Colli, S., Paoletti, R. (1987). In Vitro Effects of Iloprost on Platelet Aggregation in Normal and Hypercholesterolemia Subjects. In: Gryglewski, R.J., Stock, G. (eds) Prostacyclin and Its Stable Analogue Iloprost. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-71499-3_5
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DOI: https://doi.org/10.1007/978-3-642-71499-3_5
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