Pathophysiology

Chronic hypertension results from cumulative abnormalities in systems regulating blood pressure:

• Renin-angiotensin-aldosterone system (RAAS)
• Sympathetic nervous system
• Sodium/volume handling
• Arterial function
• Local vascular autoregulation

Key effects of these abnormalities:

• Hyperactivity of the RAAS leads to vasoconstriction, sodium retention, and volume expansion
• Increased sympathetic tone raises heart rate, contractility, and peripheral vascular resistance
• Impaired pressure-natriuresis relation causes plasma volume expansion
• Endothelial dysfunction reduces nitric oxide and vasodilation
• Arterial stiffness blunts Windkessel effect increasing pulse pressure
• Small vessel thickening and narrowing increases peripheral resistance

Disease progression:

• Early in disease, high cardiac output maintains organ perfusion against elevated resistance
• With time, increased peripheral resistance is primary cause of elevated blood pressure
• Vascular and cardiac remodeling can further exacerbate blood pressure elevation
• In most cases, combination of abnormalities in regulatory systems leads to chronic elevation in blood pressure without clear underlying cause