The interaction between the plasma KKS and RAS. Plasma kallikrein converts prorenin to renin, and renin has the ability to convert angiotensinogen to angiotensin I. Angiotensin-converting enzyme (ACE) converts inactive angiotensin I to the vasoconstrictor angiotensin II. Angiotensin II stimulates plasminogen activator inhibitor 1 (PAI1) release from endothelial cells. At the same time ACE degrades bradykinin into bradykinin_(1–7) (not shown) or bradykinin_(1–5), a peptide with thrombin inhibitory activity. PRCP is the enzyme that degrades angiotensin II or angiotensin I to the vasodilating peptide, angiotensin II_(1–7). Angiotensin II_(1–7) stimulates NO and PGI₂ formation, which potentiates the effects of bradykinin. PRCP also has the ability to convert PK to kallikrein. Formed kallikrein digests kininogens to liberate bradykinin, leaving a kinin-free kininogen (HKa) that has anti-proliferative and anti-angiogenic properties. Thus, PRCP, the same enzyme that degrades the vasoconstrictor angiotensin II, leads to the increased formation of the vasodilators bradykinin and angiotensin II_(1–7). Finally, the resulting bradykinin stimulates tPA, NO, and PGI₂ formation, thus counterbalancing the prothrombotic effect of angiotensin II.