Blood pressure and fluid and electrolyte homeostasis is regulated by the renin–angiotensin–aldosterone system.
Renin, an enzyme released from the kidneys, converts the inactive plasma protein angiotensinogen into angiotensin I (Ang I).  Then Ang I is converted to Ang II with angiotensin converting enzyme (ACE), see figure 2. Ang II in plasma then binds to AT-receptors.
ARBs are blocking the last part of the renin–angiotensin pathway and block the pathway more specifically than ACE inhibitors.
The AT receptor mediates Ang II to cause increased cardiac contractility, sodium reabsorption and vasoconstriction which all lead to increased blood pressure. By blocking AT receptors, ARBs lead to lower blood pressure.
An insurmountable inhibition of the AT receptor is achieved when the maximum response of Ang II cannot be restored in the presence of the ARB, no matter how high the concentration of Ang II is.
The angiotensin receptor blockers can inhibit the receptor in a competitive surmountable, competitive insurmountable or noncompetitive fashion, depending upon the rate at which they dissociate from the receptor.