Mechanism for thromboprotection in Bdkrb2^−/− mice. In the absence of B2R, AngII and Ang-(1-7) are elevated in plasma (Figure 1D).³  Ang-(1-7) is the ACE2 breakdown product of AngII. AngII and Ang-(1-7) interact with overexpressed AT2R and Mas receptors, respectively, to increase intravascular NO and prostacyclin. Elevation of plasma prostacyclin and NO influences vascular function, reduces platelet sensitivity to collagen-like agonists, CRP or convulxin, with reduced GPVI activation, and induces a platelet spreading defect on collagen, GFOGER, and fibrinogen. These latter effects on platelets produce a long bleeding time and contribute to the delayed thrombosis in Bdkrb2^−/− mice. Interference with AT2R,³  Mas (present report), or combined NO and prostacyclin production (3, present study) normalizes arterial thrombosis potential in Bdkrb2^−/− mice. These studies indicate in part how prostacyclin and NO regulates arterial thrombosis risk.