HTN Mechanisms

Blood pressure is determined by the equation: BP = Cardiac Output × Systemic Vascular Resistance (SVR). CO = Heart Rate × Stroke Volume. HTN results from increased CO, increased SVR, or both. Essential (primary) HTN (90-95% of cases) involves multiple interacting mechanisms: (1) RAAS activation — angiotensin II is a potent vasoconstrictor that increases SVR, stimulates aldosterone secretion (sodium/water retention → increased CO), promotes cardiac and vascular remodeling, and stimulates thirst and ADH release; (2) Sympathetic nervous system overactivity — increased norepinephrine causes vasoconstriction (alpha-1 receptors), increased heart rate and contractility (beta-1 receptors), and renin release from the juxtaglomerular apparatus; (3) Endothelial dysfunction — reduced nitric oxide (NO) bioavailability impairs vasodilation, while increased endothelin-1 promotes vasoconstriction; oxidative stress and inflammation perpetuate endothelial injury; (4) Renal sodium handling — Guyton's pressure natriuresis model: the kidney's ability to excrete sodium at a given pressure is impaired, requiring higher pressures to maintain sodium balance; (5) Vascular remodeling — chronic pressure elevation causes arteriolar wall thickening (increased media-to-lumen ratio), further increasing SVR in a self-perpetuating cycle. Secondary HTN (5-10%) has identifiable causes: primary aldosteronism...