The RAAS regulates blood pressure and fluid-electrolyte balance.

Angiotensin-converting enzyme or ACE, found abundantly in the lungs, converts angiotensin  I to angiotensin II, a potent vasoconstrictor that narrows blood vessels.

The constricted vessels compel the heart to intensify pumping, elevating blood pressure.

Angiotensin II stimulates aldosterone production, triggering sodium and water reabsorption from urine and increasing blood volume and pressure.

Bradykinin, an endogenous vasodilator, releases nitric oxide and prostacyclin, relaxing blood vessels to manage hypertension. However, ACE can inhibit bradykinin, reducing its vasodilatory impact.

ACE inhibitors like lisinopril slow bradykinin degradation, increasing its availability for vasodilation and reducing blood pressure.

ACE inhibitors also block the conversion of angiotensin I to angiotensin II. Reduced angiotensin II levels dilate blood vessels, lowering blood pressure.

The decrease in angiotensin II also curtails aldosterone production, promoting sodium and water excretion by the kidneys, further reducing blood volume and pressure.