Hypertension results from increased systemic vascular resistance (SVR), increased cardiac output, or both. At the cellular level, endothelial dysfunction reduces nitric oxide (NO) bioavailability, shifting the balance toward vasoconstrictors (endothelin-1, thromboxane A2, angiotensin II). Vascular smooth muscle cells undergo hypertrophy and hyperplasia, increasing vessel wall thickness and reducing lumen diameter. The renin-angiotensin-aldosterone system (RAAS) plays a central role: juxtaglomerular cells release renin in response to decreased renal perfusion, sympathetic activation, or decreased sodium delivery to the macula densa. Renin cleaves angiotensinogen to angiotensin I, which is converted to angiotensin II by ACE in pulmonary endothelium. Angiotensin II causes direct vasoconstriction, stimulates aldosterone secretion (sodium and water retention), promotes cardiac remodeling, and activates sympathetic nervous system. Sustained hypertension leads to arteriolar sclerosis, left ventricular hypertrophy, nephrosclerosis, and accelerated atherosclerosis. The ACC/AHA 2017 guidelines redefined hypertension as BP >= 130/80 mmHg (replacing the JNC 8 threshold of 140/90), based on evidence that cardiovascular risk increases continuously above 115/75 mmHg.