Angiotensin II of the renin-angiotensin-aldosterone system binds to G_q protein‐coupled AT₁ receptors in vascular smooth muscle, activating phospholipase  C.

This releases IP₃ and DAG, leading to myosin light chain phosphorylation and actin-myosin interaction.

These actions cause smooth muscle contraction and blood vessel constriction,  increasing peripheral resistance and blood pressure.

AT₁ receptor activation also stimulates aldosterone secretion, promoting sodium and water retention in the kidneys and increasing blood volume and pressure.

ARBs like losartan and valsartan are used to treat high blood pressure.

They compete with angiotensin II for the AT₁ receptor and deactivate it, reducing vasoconstriction. As the blood vessels dilate, the peripheral resistance decreases, and the blood pressure reduces.

The AT₁ receptor blockade also decreases aldosterone secretion, reducing sodium and water reabsorption and lowering blood volume and pressure.

Unlike ACE inhibitors, ARBs don't affect bradykinin levels, preventing dry cough.