Fig. 1
From: Angiotensin converting enzyme defects in shock: implications for future therapy
Proposed biofeedback mechanism. a Endothelial injury causes disruption of the normal renin-angiotensin-aldosterone system (RAAS) pathway via depleted ACE functionality, resulting in reduction of angiotensin II, increased production of renin, and ultimately increased ACE precursors. b With the addition of exogenous angiotensin II, a biofeedback mechanism is triggered via engagement of the angiotensin II type 1 receptor, resulting in increased blood pressure and decreased production of angiotensinogen and/or renin, ultimately reducing angiotensin I levels, ADH antidiuretic hormone