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