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The vascular tree is not a passive plumbing system. Each class of blood vessel is structurally specialised for the hydraulic and exchange roles it must perform at a particular point along the pressure cascade from the aortic root, where left ventricular ejection produces ~120 mmHg systolic pressure, to the right atrium, where pressure approaches zero. Arteries withstand and smooth high pressure; arterioles regulate flow distribution and dissipate most of the systemic pressure gradient; capillaries exchange materials with tissue across a single endothelial layer; venules and veins return blood at low pressure with the help of skeletal-muscle pumping and one-way valves. Between the capillary and the surrounding cells lies a hydraulic micro-environment — tissue fluid — formed and reabsorbed across capillary walls under the competing influences of hydrostatic and oncotic pressures, with the lymphatic system returning the small residual fraction to the circulation. This lesson maps blood vessel structure to function, derives tissue fluid formation from first principles using the Starling framework, and explains the four major causes of oedema. It is the natural companion to lessons 5 (heart and cardiac cycle) and 6 (haemoglobin and oxygen transport) — the trio that constitutes the AQA mass-transport-in-animals exam package.
This lesson maps to AQA 7402 Section 3.3.4 — Mass transport in animals (blood vessels and tissue fluid) (refer to the official AQA specification document for exact wording). The specification requires that students understand the structure and function of arteries, arterioles, capillaries, venules and veins, the formation and return of tissue fluid, and the relationship between these processes and the circulation.
Mean arterial pressure at the aorta is ~95 mmHg in a healthy young adult. By the venae cavae, mean pressure has fallen to ~3 mmHg. Almost all of this pressure drop occurs in the arterioles — the major resistance vessels — and a smaller residual drop in the capillary bed. This pressure cascade is the organising principle for blood vessel structure: vessels upstream of the arterioles must withstand high pressure; vessels downstream must operate at low pressure; capillaries must allow exchange while preserving the integrity of the column.
| Vessel | Approximate mean pressure | Wall thickness | Lumen diameter | Primary role |
|---|---|---|---|---|
| Aorta | 95 mmHg | thick | 25 mm | conduit / elastic recoil |
| Large artery | 90 mmHg | thick | 4 mm | conduit |
| Arteriole | 60 → 30 mmHg | muscular | 30 μm | resistance / flow regulation |
| Capillary | 30 → 10 mmHg | single endothelial cell | 5–10 μm | exchange |
| Venule | 10 mmHg | thin | 30 μm | collection / leukocyte trafficking |
| Vein | 5 mmHg | thin, valved | 5 mm | reservoir / return |
Arteries carry blood away from the heart. They are structurally adapted to high, pulsatile pressure.
The wall of every artery has three concentric layers. The outermost tunica externa (adventitia) is connective tissue containing collagen fibres and small vasa vasorum that supply the wall itself. The middle tunica media is the thickest layer and contains circumferentially arranged smooth muscle and elastic fibres (elastin). The innermost tunica intima is a single layer of endothelial cells on a basement membrane, with a thin internal elastic lamina beneath.
Elastic arteries (the aorta and its first few branches) have a media dominated by elastin. They distend during systole (storing some of the stroke volume as elastic potential energy in the wall) and recoil during diastole (returning that energy to drive forward flow). This elastic recoil smooths the pulsatile output of the ventricle into a more continuous arterial flow — the Windkessel effect (paraphrase the framework — no verbatim quote). Without elasticity, capillary flow would be entirely systolic and absent during diastole.
Muscular arteries (the named arteries: brachial, femoral, renal etc.) have media dominated by smooth muscle. They distribute blood to organs and contribute to vasoconstriction under sympathetic control. With age, elastic arteries stiffen (elastin is replaced by collagen), pulse pressure widens, and isolated systolic hypertension develops — the commonest blood-pressure disorder in elderly populations.
Arterial lumen is relatively narrow for the wall thickness, helping maintain pressure. Arteries do not have valves except for the aortic and pulmonary semilunar valves at the ventricular outflow — these are the only intra-arterial valves in the body, and they are at the great-artery roots, not along their length.
Arterioles are the principal resistance vessels and the major regulators of regional blood flow. Each arteriole is a few hundred micrometres long, has a media of one to three layers of smooth muscle, and innervates capillary beds downstream. Constriction or dilation of the arteriolar smooth muscle changes the lumen radius; because resistance is inversely proportional to the fourth power of radius (Poiseuille's law — paraphrase only), small radius changes produce large flow changes. Arteriolar tone is therefore the single most important variable for controlling tissue perfusion.
Arteriolar smooth muscle is responsive to many local signals. Low PO₂, high CO₂, high H⁺, high K⁺, adenosine and the inflammatory mediators NO (nitric oxide), histamine, prostaglandins all promote relaxation (vasodilation). These are the conditions of an active or stressed tissue, so the local response is demand-led vasodilation that increases flow precisely where it is needed. This integrates with the Bohr-shift O₂ unloading mechanism described in lesson 6 — both are demand-led delivery mechanisms operating at the molecular and the macroscopic level.
Sympathetic noradrenergic fibres innervate arteriolar smooth muscle (predominantly α₁-adrenergic) and produce vasoconstriction; this is the major efferent arm of the baroreflex and the body's main means of redistributing blood (e.g. away from skin and gut during exercise; away from skeletal muscle during the cold-pressor response). Parasympathetic contribution is minor (relevant in specific beds — salivary glands, genitals).
In some tissues a ring of smooth muscle at the entry to each capillary — a pre-capillary sphincter — provides additional fine control of perfusion. The sphincter opens and closes rhythmically (vasomotion), recruiting individual capillaries on demand. Recruitment is the main mechanism by which an exercising muscle increases its perfused capillary surface area by ten- to twenty-fold above the resting baseline.
Capillaries are the exchange vessels. They are too narrow to admit a red blood cell undeformed — diameters of 5–10 μm against an 8 μm red cell — so red cells squeeze through single file, maximising surface contact with the endothelium. The wall is a single layer of endothelial cells on a basement membrane; there is no smooth muscle, no elastic, no adventitia. The total length of capillaries in the adult is estimated at ~60,000 km; the total surface area is ~600 m². No tissue cell is more than ~20–40 μm from a capillary.
A-Level depth recognises three structural types of capillary.
The variation is functional: the blood-brain barrier protects neurons from circulating insults; the glomerular fenestration is the first step of urine formation; sinusoids permit hepatic albumin synthesis to enter circulation.
Three transport mechanisms operate. Diffusion of small lipophilic molecules (O₂, CO₂) occurs across the whole capillary surface, driven by concentration gradients. Diffusion of water-soluble small molecules (glucose, amino acids, ions) occurs through the intercellular clefts or fenestrations. Bulk flow (filtration and reabsorption) of water and dissolved solutes occurs by hydrostatic and oncotic forces; this is the focus of tissue-fluid formation. Transcytosis of large molecules in vesicles is a minor route.
Blood leaves capillaries into post-capillary venules, where leukocytes selectively exit the circulation during inflammation (the venule wall expresses adhesion molecules — synoptic with Section 3.2 immunology). Venules merge into veins.
Veins have the same three concentric layers as arteries but the media is much thinner and the lumen wider. The wall is more compliant (a vein at the same pressure contains more blood than an artery of the same diameter), so veins act as the body's main blood reservoir — ~65 % of total blood volume sits in the venous system at any moment.
Veins below the level of the heart contain one-way valves at intervals of a few centimetres, formed by paired pocket-shaped folds of the tunica intima. Blood flowing toward the heart pushes the valve cusps open; any backflow pushes them shut. Valves prevent gravitational pooling and ensure unidirectional flow.
Venous return depends not on the heart but on auxiliary mechanisms. The skeletal muscle pump — rhythmic contraction of leg muscles during walking — squeezes deep veins, propelling blood toward the heart between functional valves. The respiratory pump — alternating intra-thoracic and intra-abdominal pressures during breathing — also drives venous return. Prolonged immobility (long-haul flights, hospital bedrest) loses both pumps and predisposes to deep vein thrombosis.
| Feature | Artery | Arteriole | Capillary | Venule | Vein |
|---|---|---|---|---|---|
| Wall thickness | thick | moderate | very thin | thin | thin |
| Tunica media | thick elastin or muscle | smooth muscle | absent | thin | thin |
| Lumen | narrow | narrow | very narrow | wider | wide |
| Pressure | high, pulsatile | falling | low | very low | low |
| Valves | only at heart outlet | none | none | none | yes |
| Function | conduit | resistance / regulation | exchange | collection | return / reservoir |
Capillary walls leak. Plasma fluid filters out at one end of the capillary, bathes the surrounding cells as tissue fluid (interstitial fluid), and most of it is reabsorbed at the other end of the same capillary or via the lymphatics. The balance of filtration and reabsorption is determined by the interplay of two pressures.
Hydrostatic pressure is the physical pressure exerted by the blood on the capillary wall. At the arteriolar end of a typical capillary, hydrostatic pressure is ~4.5 kPa (~33 mmHg). It drives fluid out of the capillary into the interstitium. Hydrostatic pressure falls along the capillary length, reaching ~1.5 kPa (~12 mmHg) at the venule end as friction dissipates energy.
Plasma contains plasma proteins — predominantly albumin (~40 g L⁻¹), with globulins and fibrinogen. The proteins are too large to cross the capillary wall (except in sinusoids). They generate a colloid osmotic pressure — oncotic pressure — of ~3.4 kPa (~25 mmHg) that draws water back into the capillary. Oncotic pressure is approximately constant along the capillary length because protein concentration changes negligibly during transit (only a few percent of plasma water is filtered).
At the arteriolar end: net outward force = hydrostatic (4.5 kPa) − oncotic (3.4 kPa) = +1.1 kPa outward. Fluid filters out, carrying dissolved small solutes (glucose, amino acids, urea, salts) but not proteins or cells. This is ultrafiltration.
At the venule end: net outward force = hydrostatic (1.5 kPa) − oncotic (3.4 kPa) = −1.9 kPa, i.e. +1.9 kPa inward. Fluid is reabsorbed.
Approximately 90 % of filtered fluid is reabsorbed at the venous end of the same capillary. The remaining ~10 % drains into the lymphatic capillaries that originate blindly in the interstitium, is processed through lymph nodes, joins the thoracic duct (and the right lymphatic duct), and returns to venous blood at the subclavian veins. About 2–4 L of lymph is returned per day in a 70 kg adult.
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