RAAS Inhibitors

Introduction

• The renin-angiotensin system (RAS/RAAS) is the dominant long-term regulator of blood pressure, Na⁺/K⁺ balance, extracellular fluid volume and cardiovascular remodeling; its dysregulation drives hypertension, heart failure, post-MI remodeling, diabetic nephropathy and CKD.
• Angiotensin II (AngII), an octapeptide, is the principal effector — on a molar basis ≈40× more potent a pressor than noradrenaline. RAS-blocking drugs are therefore among the most-used cardiovascular agents.
• Four points of pharmacological interruption — Renin (direct renin inhibitors), the AngI→AngII step (ACE inhibitors), the AT₁ receptor (ARBs), and a combined AT₁-block + natriuretic-peptide-sparing strategy (ARNI); aldosterone-receptor antagonists and β₁-blockers also suppress the RAS but are covered elsewhere.
• All RAS inhibitors share a common footprint — antihypertensive, cardioprotective (heart failure, post-MI) and renoprotective (proteinuric/diabetic nephropathy) — but differ in how they perturb individual RAS components (see comparison figure).