The renin-angiotensin-aldosterone system, or RAAS, involves numerous enzymes and hormones.

Here, the angiotensin-converting enzyme or ACE converts angiotensin I to angiotensin II. Angiotensin II binds to AT₁ receptors, triggering vasoconstriction and aldosterone secretion.

Aldosterone promotes renal sodium and water reabsorption, increasing blood volume and pressure.

An overactive RAAS raises angiotensin II levels, causing hypertension. Treatments target different stages of this pathway to control it effectively.

ARBs block angiotensin II from binding to AT₁ receptors, while ACE inhibitors prevent angiotensin II production. So, they both effectively reduce blood pressure.

However, since the ACE-independent pathways mediated by chymase or cathepsin G enzymes continue converting angiotensin I to II, inhibiting the initial step is crucial for managing hypertension.

Direct renin inhibitors inhibit renin directly and prevent the conversion of angiotensinogen into angiotensin I.

This, in turn, reduces angiotensin II production, decreasing the blood volume and pressure.