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Hypertension—sustained elevation of systemic arterial pressure—damages target organs through increased wall stress and chronic inflammation. Essential hypertension involves complex interactions of neurogenic, renal, and endocrine factors; secondary hypertension has identifiable causes.
Distinguish primary from secondary hypertension by clinical clues. Map hypertension-induced organ damage: left ventricular hypertrophy and diastolic dysfunction (heart), membranous glomerulonephritis (kidney), retinal hemorrhage (eye).
White-coat hypertension is clinically significant—it increases risk. 'Normal' systolic pressure (<120 mmHg) does not exclude diastolic dysfunction or target organ damage.
From your study of blood pressure regulation, you know that arterial pressure is determined by cardiac output and systemic vascular resistance, governed by the baroreceptor reflex, RAAS, and the sympathetic nervous system. In a healthy individual these systems maintain pressure in a tight range. Hypertension is the sustained failure of this regulation, with systolic pressure ≥130 mmHg or diastolic ≥80 mmHg by current guidelines. But more important than the number is understanding *why* it persists and what it does to the body over time.
Essential (primary) hypertension accounts for ~90% of cases and has no single identifiable cause. Instead, it reflects the cumulative effect of genetic predisposition, dietary sodium excess, obesity-driven sympathetic activation, and RAAS upregulation — the system you learned about in RAAS. Excess dietary sodium raises extracellular fluid volume; the kidneys in hypertensive individuals set a higher "pressure-natriuresis" threshold, requiring higher pressure to excrete the same sodium load. Obesity activates the sympathetic nervous system through leptin and adipokines, raising heart rate and vascular tone. These inputs reinforce each other, shifting the setpoint for pressure homeostasis upward. Secondary hypertension (~10%) has a specific cause: renal artery stenosis activates RAAS chronically (Goldblatt hypertension), primary hyperaldosteronism causes sodium retention independent of angiotensin II, and pheochromocytoma secretes catecholamines episodically.
The damage that sustained high pressure causes to blood vessels follows directly from physics. Wall stress (tension per unit area) in a vessel is proportional to pressure times radius (Laplace's law). Chronically elevated pressure subjects arterial walls to abnormal mechanical stress, triggering a maladaptive remodeling cascade. Vascular smooth muscle cells hypertrophy and synthesize more extracellular matrix. The intimal endothelium, damaged by turbulent high-pressure flow, becomes dysfunctional — expressing adhesion molecules, reducing nitric oxide synthesis, and promoting inflammation. This is the beginning of arteriolosclerosis: arteriolar walls thicken, the lumen narrows, and resistance rises further, perpetuating the pressure elevation in a vicious cycle.
End-organ damage follows the distribution of the circulation. In the heart, the left ventricle pumps against elevated afterload and compensates with left ventricular hypertrophy (LVH). Initially adaptive, LVH stiffens the ventricle, impairing diastolic filling and eventually reducing systolic function — the path to heart failure. In the kidney, afferent arteriolar hyalinosis (protein deposits from plasma forced into thickened walls) impairs glomerular autoregulation, exposing glomeruli to high pressure. Glomerulosclerosis and proteinuria result, progressively reducing GFR. Hypertension and CKD amplify each other: damaged kidneys retain sodium, raising pressure further. In the brain, chronic endothelial dysfunction and wall thickening of small cerebral arterioles sets the stage for lacunar infarcts (small-vessel strokes) and hypertensive encephalopathy. In the retina, the same arteriolar changes are directly visible on fundoscopy — copper-wiring, AV nicking, flame hemorrhages — making the eye a window into vascular end-organ damage elsewhere.
The therapeutic logic of antihypertensive drugs maps directly onto the physiology. ACE inhibitors and ARBs block RAAS, reducing angiotensin II–mediated vasoconstriction and aldosterone-mediated sodium retention. Calcium channel blockers relax smooth muscle in arteriolar walls, directly reducing resistance. Thiazide diuretics reduce plasma volume by blocking sodium reabsorption in the distal tubule. Beta-blockers reduce cardiac output by slowing heart rate and contractility. Each drug class attacks a different mechanistic lever, which is why combination therapy is often more effective than single-agent therapy at maximum dose. The goal is not just to lower the number — it is to reduce wall stress, allow vascular remodeling to reverse, and slow the progression of end-organ damage before it becomes irreversible.