Aspirin vasoconstrictor effects

Because TXA2 is a potent vasoconstrictor as well as a labile platelet aggregation inducer, inhibition of production of TXA2 effectively blocks platelet aggregation. Aspirin and related analogues (Fig. 31.15) exhibit their effectiveness through such a blocking mechanism. 

However, concerns have been voiced regarding the prothrombotic properties of COX-2 inhibitors. Aspirin has been shown to permanently inactivate platelet COX-1 and to suppress TXA production but, at the same time, has little effect on the synthesis of PGI. Tliis is considered as the main mechanism explaining its antithrombotic effects and is the basis of the use of low-dose aspirin to prevent thromboembohc events. Conversely, selective COX-2 inhibitors suppress platelet-inhibitory PGI production without inhibiting the vasoconstrictor TXA, thus favouring the production of prothrombotic prostanoids. This leads to a plausible mechanism by which COX-2 inhibitors may enhance the risk of thrombosis in otherwise predisposed individuals (Mukherjee, 2002 Patrono et al, 2001). 

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