The renin-angiotensin-aldosterone system (RAAS) is a central hormonal cascade in blood pressure regulation. When renal perfusion drops, juxtaglomerular cells release renin, which cleaves angiotensinogen (from the liver) to angiotensin I. Angiotensin-converting enzyme (ACE), primarily in pulmonary endothelium, converts angiotensin I to angiotensin II (AT-II). AT-II acts on AT1 receptors to cause potent arteriolar vasoconstriction, stimulate aldosterone release from the adrenal cortex (increasing Na+/water reabsorption in the collecting duct via ENaC), promote ADH release, stimulate thirst, and induce cardiac and vascular remodeling (hypertrophy and fibrosis). ACE also degrades bradykinin, a vasodilator; ACE inhibitors therefore increase bradykinin (explaining both their vasodilatory benefit and the dry cough side effect). Endothelial dysfunction occurs when chronic hypertension reduces nitric oxide (NO) synthesis and increases endothelin-1, reactive oxygen species, and inflammatory cytokines, promoting atherosclerosis and further vascular stiffening.