What is the mechanism of action of angiotensin receptor blockers (ARBs)?

Angiotensin receptor blockers (ARBs) primarily work by blocking angiotensin II receptors, specifically the AT1 subtype. Angiotensin II is a potent vasoconstrictor and plays a significant role in increasing blood pressure and promoting sodium retention through aldosterone secretion. By inhibiting the action of angiotensin II at its receptors, ARBs lead to vasodilation, reduced blood pressure, decreased cardiac workload, and improved outcomes in conditions like hypertension and heart failure.

The mechanism is targeted, as it directly interferes with the pathway that contributes to increased vascular resistance and fluid retention. Moreover, unlike ACE inhibitors, ARBs do not lead to an accumulation of bradykinin, an effect that can be associated with cough or angioedema. This makes ARBs a valuable option for patients who may not tolerate ACE inhibitors well.

Other options presented do not accurately describe the primary action of ARBs. For instance, while inhibiting renin secretion is a component of the broader renin-angiotensin-aldosterone system (RAAS) regulation, it is not the direct action of ARBs. Blocking calcium channels is more characteristic of calcium channel blockers, which act through a different mechanism involving smooth muscle relaxation. Inhibition of