ARBs — Clinical Use & Key Differences

Angiotensin II receptor blockers (ARBs — losartan, valsartan, irbesartan, candesartan) block angiotensin II at the AT1 receptor rather than preventing its formation. This distinction matters: ACE inhibitors block the enzyme that converts angiotensin I to II, which also causes bradykinin to accumulate. ARBs skip that enzyme entirely, so bradykinin does not build up — which is why the dry cough and angioedema risk seen with ACE inhibitors are significantly reduced (though a small residual angioedema risk remains, especially in patients with prior ACE inhibitor-induced angioedema). Indications overlap heavily with ACE inhibitors: hypertension, heart failure with reduced ejection fraction, diabetic nephropathy (particularly losartan and irbesartan for type 2 diabetic nephropathy), and post-MI left ventricular dysfunction. ARBs are first-line alternatives when an ACE inhibitor is not tolerated. They are NOT combined with ACE inhibitors — dual RAAS blockade increases hyperkalemia, hypotension, and renal failure risk without added benefit. Like ACE inhibitors, ARBs are absolutely contraindicated in pregnancy (Category X equivalent — fetal renal damage and death, especially second and third trimesters). Potassium and renal function monitoring still applies because the downstream effect on aldosterone suppression is the same.