ACE inhibitors and ARBs both target the RAAS but at different points. ACEi block angiotensin-converting enzyme, preventing AT-I to AT-II conversion and simultaneously increasing bradykinin (a vasodilator normally degraded by ACE). This dual mechanism provides vasodilation but also causes the characteristic dry cough (10-15%) and rare angioedema (0.1-0.7%) via bradykinin and substance P accumulation. ARBs selectively block the AT1 receptor, preventing the vasoconstrictive, aldosterone-stimulating, and remodeling effects of AT-II regardless of its source (ACE or non-ACE pathways like chymase). ARBs do NOT affect bradykinin metabolism, explaining the absence of cough. Both classes reduce proteinuria by dilating the efferent arteriole, lowering intraglomerular pressure. Both are teratogenic and absolutely contraindicated in pregnancy. The choice between them is primarily driven by tolerability (cough with ACEi → switch to ARB) and cost considerations.