<Dl> <Dd> Asp - Arg - Val - Tyr - Ile - His - Pro-Phe </Dd> </Dl> <Dd> Asp - Arg - Val - Tyr - Ile - His - Pro-Phe </Dd> <P> Angiotensin I is converted to angiotensin II (AII) through removal of two C - terminal residues by the enzyme angiotensin - converting enzyme (ACE), primarily through ACE within the lung (but also present in endothelial cells, kidney epithelial cells, and the brain). Angiotensin II acts on the CNS to increase vasopressin production, and also acts on venous and arterial smooth muscle to cause vasoconstriction . Angiotensin II also increases aldosterone secretion, therefore, it acts as an endocrine, autocrine / paracrine, and intracrine hormone . </P> <P> ACE is a target of ACE inhibitor drugs, which decrease the rate of angiotensin II production . Angiotensin II increases blood pressure by stimulating the Gq protein in vascular smooth muscle cells (which in turn activates an IP3 - dependent mechanism leading to a rise in intracellular calcium levels and ultimately causing contraction). In addition, angiotensin II acts at the Na / H exchanger in the proximal tubules of the kidney to stimulate Na reabsorption and H excretion which is coupled to bicarbonate reabsorption . This ultimately results in an increase in blood volume, pressure, and pH . Hence, ACE inhibitors are major anti-hypertensive drugs . </P>

Where does the conversion of angiotensin i to angiotensin ii occur