Give overview of local blood control according to guyton and halls physiology
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Local Blood Flow Control - Guyton and Hall Textbook of Medical Physiology
1. Fundamental Principle
Most tissues have the ability to control their own local blood flow in proportion to their specific metabolic needs. Blood flow to each tissue is normally regulated at the minimal level that will supply the tissue's requirements - no more, no less. This minimizes cardiac workload while preventing nutritional deficiency.
Tissue needs served by local blood flow:
- Delivery of oxygen
- Delivery of nutrients (glucose, amino acids, fatty acids)
- Removal of CO2
- Removal of H+ ions
- Maintenance of proper ion concentrations
- Transport of hormones and other substances
2. Two Phases of Local Blood Flow Control
| Phase | Timing | Mechanism |
|---|---|---|
| Acute control | Seconds to minutes | Rapid vasodilation/vasoconstriction of arterioles, metarterioles, and precapillary sphincters |
| Long-term control | Days to weeks | Changes in physical size and number of blood vessels |
3. Acute Control
A. Metabolic Theory (Most Important)
The metabolic theory proposes that when tissue metabolic activity increases - or blood flow decreases - local tissue vasodilator substances accumulate, causing vasodilation.
Key vasodilator substances released:
- Adenosine (especially in cardiac muscle - most studied)
- CO2
- Lactic acid
- Adenosine monophosphate (AMP)
- Adenosine diphosphate (ADP)
- K+ ions
- H+ ions
When blood flow is insufficient, oxygen delivery falls, the above metabolites accumulate, and they diffuse to the precapillary sphincters and arterioles to cause vasodilation - directly increasing flow back to match demand.
B. Oxygen Demand Theory (Tissue Oxygen)
Oxygen is required for smooth muscle contraction. When oxygen delivery falls below what is needed, the smooth muscle of arterioles and precapillary sphincters relaxes (for lack of oxygen to contract), causing vasodilation. This directly links blood flow to oxygen availability.
C. Autoregulation of Blood Flow
When arterial pressure suddenly rises (e.g., from 100 to 150 mm Hg), blood flow increases almost instantly by ~100%, but within 30 seconds to 2 minutes, it returns to near baseline (only ~10-15% above normal). This is autoregulation - the tendency of blood flow to remain relatively constant despite changes in arterial pressure.
Two theories for autoregulation:
-
Metabolic theory: Increased pressure delivers excess oxygen/nutrients → vasodilator metabolites washed away → arterioles constrict → flow returns to normal.
-
Myogenic theory: Sudden stretch of the arteriolar wall (from increased pressure) directly causes reflex smooth muscle contraction (Bayliss effect), reducing the vessel diameter and normalizing flow.
D. Special Examples of Acute Metabolic Control
- Reactive hyperemia: After blood flow to a tissue is completely blocked for a period, the flow upon release is several times normal - proportional to the duration of occlusion. Caused by accumulation of vasodilator metabolites and oxygen deficit.
- Active hyperemia: When a tissue becomes highly active (e.g., exercising muscle), local vasodilators increase, causing marked increase in blood flow matched to metabolic rate.
4. Long-Term Blood Flow Regulation
Acute mechanisms alone adjust flow only about three-quarters of the way to exact tissue requirements. Long-term regulation, developing over days to weeks, achieves more precise control.
Key mechanism: Changes in vascularity (angiogenesis and vascular remodeling)
- Chronic tissue overactivity → increased oxygen demand → arterioles and capillaries increase in number and size
- Chronic inactivity → reduced blood flow → vessel numbers and sizes decrease
Vascular Endothelial Growth Factor (VEGF): When tissue oxygen delivery is chronically insufficient, cells release VEGF, which stimulates growth of new blood vessels (angiogenesis). This is the primary mechanism for long-term flow matching.
Collateral circulation: In ischemic tissues, existing small vessels enlarge and new collaterals form to bypass obstruction. This is important in coronary artery disease, where collaterals can restore partial flow.
Key point: Once long-term regulation has occurred, changes in arterial pressure between 50 and 200 mm Hg have very little effect on tissue blood flow - demonstrating the extreme effectiveness of this mechanism.
5. Humoral Control of Local Blood Flow
Vasodilator Substances:
| Substance | Source | Mechanism |
|---|---|---|
| Bradykinin | Kallikrein acting on kininogen | Potent vasodilator; increases capillary permeability |
| Histamine | Mast cells, basophils | Vasodilates arterioles; increases capillary permeability |
| Serotonin (5-HT) | Platelets | Can vasodilate or vasoconstrict depending on vessel |
| Prostaglandins | Damaged/active tissue cells | Generally vasodilate (PGI2/prostacyclin); modulate inflammation |
Vasoconstrictors:
| Substance | Source | Mechanism |
|---|---|---|
| Angiotensin II | Liver/kidney (RAAS) | Potent vasoconstrictor; important in hypertension |
| Vasopressin (ADH) | Posterior pituitary | Extreme vasoconstriction; released in severe hemorrhage |
| Norepinephrine | Sympathetic nerves/adrenal medulla | Vasoconstriction via alpha-adrenergic receptors |
| Endothelin | Damaged endothelium | 21-amino acid peptide; one of the most potent vasoconstrictors known |
6. Endothelium-Derived Factors
The vascular endothelium plays a central local regulatory role:
Nitric Oxide (NO) - Key Vasodilator
- Produced from L-arginine by endothelial nitric oxide synthase (eNOS)
- Released in response to: shear stress (blood flow), acetylcholine, bradykinin, histamine
- Acts on vascular smooth muscle via cGMP pathway → relaxation → vasodilation
- Clinical relevance: Sildenafil (Viagra) inhibits PDE-5, prolonging cGMP and the vasodilatory action of NO. Used in erectile dysfunction and pulmonary hypertension.
- Atherosclerosis impairs endothelial NO release - contributing to hypertension and coronary artery disease.
Endothelin - Vasoconstrictor
- Released when endothelium is damaged (trauma, chemicals, hypertension)
- 21-amino acid peptide; acts in nanogram amounts
- Helps prevent blood loss after vessel injury via intense local vasoconstriction
- Endothelin receptor blockers (e.g., bosentan) are used in pulmonary arterial hypertension
Summary Table
| Control Type | Mechanism | Time Course | Examples |
|---|---|---|---|
| Acute metabolic | Vasodilator metabolites (adenosine, CO2, H+) | Seconds | Exercise hyperemia, reactive hyperemia |
| Acute myogenic | Stretch-induced smooth muscle contraction | Seconds | Autoregulation |
| Humoral vasodilation | Bradykinin, histamine, NO, prostaglandins | Minutes | Inflammation, endothelium-mediated |
| Humoral vasoconstriction | Angiotensin II, ADH, endothelin, NE | Minutes | Hemorrhage, vessel injury |
| Long-term | Angiogenesis, vascular remodeling (VEGF) | Days - weeks | Collateral formation, exercise training |
Source: Guyton and Hall Textbook of Medical Physiology (ISBN 9780443111013), Chapter 17 - Local and Humoral Control of Tissue Blood Flow
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