Reciprocal regulation of human platelet function by endogenous prostanoids and through multiple prostanoid receptors

06.07.2014

Hubertus K, Mischnik M, Timmer J, Herterich S, Mark R, Moulard M, Walter U, Geiger J.

Eur J Pharmacol. 2014 Jul 6;740C:15-27

Eur J Pharmacol.        online article

Platelets are permanently exposed to a variety of prostanoids formed by blood cells or the vessel wall. The two major prostanoids, prostacyclin and thromboxane act through well established pathways mediated by their respective G-protein coupled receptors inhibiting or promoting platelet aggregation accordingly.  A mathematical model integrating the pathway components was established which successfully reproduces the observed platelet responses.