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Fig. 2 | Critical Care

Fig. 2

From: Angiotensin converting enzyme defects in shock: implications for future therapy

Fig. 2

Proposed mechanism of angiotensin metabolism during shock and with the addition of exogenous angiotensin II. a When ACE is inhibited by ACE inhibitors or during vasodilatory shock, bradykinin, angiotensin I, and angiotensin 1-7 (ANG 1-7) increase. ANG 1-7 has effects that are the opposite those of angiotensin II. Both ANG 1-7 and bradykinin are vasodilatory, and they may build up when ACE is not functional, compounding the issue of angiotensin II insufficiency. b The addition of exogenous angiotensin II provides a direct benefit by ameliorating the angiotensin II insufficiency. However, it may also provide benefit by reducing vasodilatory angiotensins via biofeedback, resulting in ACE availability and bradykinin degradation (blue lightning bolt). NEP neutral endopeptidase, PEP prolyl endopeptidase

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