🩸 Vascular Physiology: The Three Distinct Vessels
The vascular tree is not a single pipe. It is three distinct types of vessels, each with a specific structure and function. Hypertension affects each one differently.
| Vessel Type | Structure | Primary Function | Pressure Here |
|---|---|---|---|
| Arteries (Shock Absorbers) | Thick wall, high Elastin, smooth muscle. | Dampen pulse pressure via Windkessel effect (stretch & recoil). | Pulsatile (e.g., 120/80) |
| Arterioles (The Faucets) | Thick smooth muscle, low elastin, tiny radius. | Regulate flow into capillaries. Generate TPR. | Massive drop (80 → 30 mmHg) |
| Capillaries (Exchange Zone) | Single layer of endothelium. No muscle. | Gas & nutrient exchange (O2, CO2, Glucose). | Very low (20-30 mmHg) |
| Veins (Reservoirs) | Thin wall, high Collagen, highly distensible. | Hold ~60-70% of blood volume. Regulate preload. | Very low (~10 mmHg) |
The Windkessel Effect (Arterial Elasticity)
Systole: The aorta stretches to accept the bolus of blood. Diastole: The elastic recoil squeezes blood forward into the arterioles.
Pathology: In hypertension, elastin breaks down and is replaced by stiff Collagen. The aorta cannot recoil. Result: Isolated Systolic Hypertension (High top number, low bottom number).
The Arteriole: The Site of Resistance
Arterioles are the primary site of Total Peripheral Resistance (TPR). Their smooth muscle responds to:
- Myogenic Response: Stretch = Constriction (protects capillaries).
- Sympathetic Nerves: Norepinephrine binds Alpha-1 → Constriction.
- RAAS: Angiotensin II binds AT1 → Constriction.
Chronic Remodeling: Sustained high pressure causes the arteriole wall to thicken (hypertrophy) and lay down collagen. The lumen narrows permanently, locking in high TPR.
The Veins: The Volume Reservoir
Veins are highly compliant. If they constrict (venoconstriction), they squeeze blood back to the heart, increasing Preload and Stroke Volume. This is why heart failure patients get edema—the veins are backed up with volume.