ACE inhibitors inhibit ACE which prevents the formation of angiotensin II and prevents angiotensin-induced vasoconstriction to decrease blood pressure which prevents angiotensin-induced released of aldosterone to decreased sodium and water retention which further decrease blood pressure

ACE inhibitors inhibit ACE which prevents the formation of angiotensin II and prevents angiotensin-induced vasoconstriction to decrease blood pressure which prevents angiotensin-induced released of aldosterone to decreased sodium and water retention which further decrease blood pressure. ACE inhibitor prevents the formation of Angiotensin II which prevents vasoconstriction and decreased blood volume by aldosterone (vasopressin) to decrease salt and water reabsorption into the blood. Therefore, blood volume remains the same and does not increase blood pressure. In the Renin Angiotensin Aldosterone system, Angiotensin II is produced by the base compound Angiotensinogen which is made in the liver and is acted upon by Renin (located in the kidney) to form Angiotensin I. Angiotensin I, is act upon by Angiotensin Converting Enzyme and Angiotensin II is formed. Angiotensin II has the following reactions; it increases Sympathetic transmission by increasing heart rate and vasoconstriction. It also increases Vasopressin which is also known as an Antidiuretic hormone. Vasopressin acts on the kidney by increasing salt and water permeability in the cells located in distal convoluted tubule and collecting duct thereby the absorption of salt and water into the blood occurs which increase blood volume and urine output. Angiotensin II is also a vasoconstrictor that shown in the kidney (efferent arteriole of the juxtaglomerular apparatus) it reduces blood flow to the kidneys, by decreasing Glomerular filtration rate, decreasing urinary output and increases blood volume (Grossman and Porth, 2014). Angiotensin II also affect Aldosterone release which increases salt and water reabsorption into the blood which increases potassium secretion, decreasing urine output and increasing blood volume. With all this increase in blood volume, the blood increases. Therefore ACE inhibitor, inhibits Angiotensin-converting Enzyme and therefore no Angiotensin II is produced, and so there is no vasoconstriction, no vasopressin or aldosterone formation or no sodium or water resorption in the blood, and the blood volume remains the same, and so the blood pressure does not increase. There is also a vasodilation effect that ACE inhibitor does which is inhibiting bradykinin degradation, and then prostaglandin production is stimulated.