Essential hypertension - classification, etiology, and pathogenesis.
Essential (primary) hypertension is sustained elevation of systemic arterial blood pressure, usually defined as:
- ≥140/90 mmHg (based on repeated measurements),
- Without an identifiable secondary cause.
It accounts for ~90–95% of all hypertension cases.
Classification
Based on severity (JNC and ESC guidelines)
Based on progression
- Benign hypertension: slowly progressive, asymptomatic for years.
- Malignant (accelerated) hypertension: rapid rise in BP (>180/120 mmHg), with end- organ damage.
Etiology
- Multifactorial (complex interplay):
- Genetic predisposition:
- Family history; polygenic inheritance.
- Variations in renin-angiotensin-aldosterone system (RAAS) components.
- Environmental factors:
- High salt intake.
- Obesity.
- Physical inactivity.
- Excess alcohol consumption.
- Stress.
- Other contributing factors:
- Insulin resistance and metabolic syndrome.
- Aging (arterial stiffness).
Pathogenesis
- 1 Increased peripheral vascular resistance (PVR)
- Functional or structural narrowing of arterioles.
- This narrowing happens due to stronger vasoconstrictor signals (e.g., catecholamines, angiotensin II) and less vasodilator activity.
- Endothelial dysfunction reduces nitric oxide availability, favoring vasoconstriction → overall higher PVR → higher blood pressure.
- 2 Abnormal sodium handling
- Reduced renal sodium excretion (either due to genetic predisposition or hormonal influences. ) → increased plasma volume → increased cardiac output → hypertension.
- 3 Overactivity of RAAS
- Increased renin secretion (some patients) even without obvious triggers.
More angiotensin II → vasoconstriction, aldosterone-mediated sodium retention.
- 4 Sympathetic nervous system overactivity
Enhanced sympathetic tone → increased heart rate, cardiac output, vasoconstriction.
- 5 Vascular remodeling
Chronic high pressure leads to smooth muscle hypertrophy in arterioles → fixed increased PVR → maintenance of high BP even if initial triggers lessen.