Platelets of humans with type 2 diabetes (DM2) exhibit fewer prostacyclin receptor (IPR) binding sites as well as decreased iloprost (ILO)‐mediated cAMP accumulation

Humans with DM2 exhibit enhanced platelet aggregation that has been suggested to result from increased synthesis of the proaggregatory prostanoid, thromboxane by platelets, as well as from increased platelet thromboxane receptor sensitivity. The proaggretory effects of thromboxane are opposed by the antiaggregatory prostanoid, prostacyclin, released from the endothelium. Platelets express the prostacyclin receptor (IPR) and it has been suggested that reduced IPR activity may contribute to increased thromboxane sensitivity in DM2. Here we investigated the hypothesis that platelets of humans with DM2 exhibit decreased IPR expression as well as reduced responsiveness to the prostacyclin analog, iloprost (ILO) when compared to healthy humans. Platelets of humans with DM2 and controls were isolated from whole blood. Using 3 H‐ILO, we determined that the number of IPR binding sites (Bmax) is reduced in platelets of humans with DM2. Furthermore, when platelets of humans with DM2 were stimulated with ILO, increases in cAMP were significantly reduced. The decreased IPR binding capacity and response to prostacyclin in platelets of humans with DM2 may contribute to the increased tendency for platelet aggregation in humans with DM2. Financial support provided by the American Diabetes Association (BS‐150).