The data from our study suggest that NO effectively, and with similar potency, inhibit both PAR1- and PAR4-mediated platelet aggregation. Thus, in the current search for new better targets for the management of thrombosis, it does not seem to be worth putting emphasis on NO as a way to differently target/affect PAR1 and PAR4. However, PAR1 and PAR4 differ in their ability to undergo desensitization. PAR1 is desensitized in cumulative dose- response studies, but not PAR4. Even more interesting, the desensitization of PAR1 does not seem to affect the activity of PAR4.

To further enhance the potential future of PAR1 and PAR4 as therapeutic targets, more studies are needed to clarify differences in their activities and mechanisms of desensitization. The results from our study, however, suggest that PAR4 may be a more suitable therapeutic target than PAR4.