Two macroscopic (gross-anatomy) sub-types
Elastic (Conducting) arteries
Muscular (Distributing) arteries
Diagram in video shows one quarter of each vessel’s cross-section, exposing all three tunics and facilitating side-by-side layer comparison.
Microscopic counterpart: arterioles (discussed later).
Alternate name: Conducting arteries – main task is simply to conduct blood from the heart to downstream vessels, not to regulate lumen size.
Examples
Aorta
Immediate branches of the aorta (brachiocephalic, common carotid, subclavian, etc.)
Pulmonary trunk & its immediate branches
General dimensions
Largest individual diameter and greatest total cross-sectional area of any artery type.
Tunica media
Thickest of the three tunics in elastic arteries.
Contains abundant elastic protein fibers (wavy blue lines in histology slide) ⇒ gives the name “elastic.”
Compliance
Definition: degree to which a vessel stretches (distends) for a given internal pressure.
Elastic arteries exhibit low compliance relative to veins: hard to stretch, small ΔV for a given ΔP.
Graph shown: compliance curve sits below venous curve – at any pressure, veins distend far more.
Analogy
Thick, tough rubber band (elastic artery) vs thin flimsy rubber band (vein).
Elastic recoil
Because they resist stretch, release of tension produces a forceful snap-back.
Functional consequence during the cardiac cycle:
Systole: LV ejection ↑ aortic pressure → wall distends (stores elastic potential energy).
Diastole: Aortic valve closes, blood flows downstream, wall recoils quickly → lumen volume ↓, pressure inside ↑ (Boyle’s law P \propto \frac{1}{V}).
Creates dicrotic notch/bump on aortic pressure curve right after semilunar valve closure.
Physiological significance: prevents diastolic arterial pressure from falling too low (helps keep MAP high enough to perfuse tissues between heartbeats).
Alternate name: Distributing arteries – deliver blood from elastic arteries to organs/tissues.
Size
Smaller diameter & lumen than elastic arteries (farther from heart).
Tunica media
Contains fewer elastic fibers, leaving space for more densely packed smooth muscle cells.
Total thickness still less than in elastic arteries but muscle density higher.
Functional capacity
Can perform modest vasoconstriction/vasodilation (more than elastic arteries but far less than arterioles).
Therefore, minor role in peripheral resistance.
Histology slide comparison shows scant wavy elastic fibers and tight smooth-muscle bundles.
Primary resistance vessels of the circulation.
Dimensions
Microscopic lumen → small absolute radius; small Δr changes translate to large ΔR (Poiseuille’s law R \propto \frac{1}{r^4}).
Tunica media
1–3 concentric layers of smooth muscle.
Cells arranged in discrete circular “ring” units ⇒ act like tiny sphincters pinching lumen diameter.
Tunica adventitia
Very thin outer connective layer.
Functional advantages
Rings allow large percent change in lumen size → powerful control over resistance and therefore blood flow.
Arterioles branch into metarterioles that thread through the center of a capillary bed.
Pre-capillary sphincters
Rings of smooth muscle (same architecture as arteriolar rings) located where metarteriole channels meet individual capillaries.
Regulate entry of blood into capillaries on a moment-to-moment basis.
Routing consequence of constriction
When sphincters close, blood bypasses true capillaries via metarteriole → venule pathway, reducing capillary perfusion.
Extrinsic (neural & hormonal)
Goal: maintain Mean Arterial Pressure (MAP) via adjusting Total Peripheral Resistance (TPR).
Sympathetic tone, epinephrine, vasopressin, angiotensin II, etc.
Intrinsic (local) controls – two key mechanisms
Metabolite-mediated (active hyperemia) – dominates in most tissues.
Myogenic response – present in select vascular beds (kidney, brain, etc.).
Trigger: ↑ metabolic activity of a tissue (e.g., contracting biceps).
Local extracellular chemistry changes
↓ O_2 (purple dots in diagram)
↑ CO_2 + ↑ H^+ (green dots) – metabolic by-products
Vascular smooth muscle senses these metabolites (act as chemical messengers)
↓ O2, ↑ CO2, ↑ H^+ ➔ smooth-muscle relaxation ➔ arteriolar dilation
Consequences
↓ Resistance (R)
↑ Blood flow (Q) through arteriole and downstream capillaries
Matches delivery of O_2 / nutrients & removal of wastes to heightened demand.
Operates continuously, making fine-tuned adjustments “in the background.”
“Myo” (muscle) + “genic” (generated) – response generated by muscle’s stretch-sensitive ion channels.
Purpose: Maintain relatively constant capillary blood flow despite changes in perfusion pressure.
Especially important in kidney (constant filtration) & brain (constant perfusion).
Mechanism (flowchart)
↑ MAP → ↑ Perfusion pressure (P) within arteriole.
↑ Distending pressure → arterial wall stretches.
Stretch-activated smooth muscle channels open → smooth muscle depolarizes → contracts.
Arteriole constricts → ↑ Resistance (R).
Goal: ΔR equals ΔP so that Q = \frac{\Delta P}{R} returns to baseline.
Response latency: 1–2 s; quickly restores steady flow.
Works in reverse: ↓ MAP → ↓ stretch → smooth muscle relaxes → dilation → keeps flow constant.
Compliance curves presented side-by-side.
For any given intraluminal pressure:
Vein undergoes large volume change (high compliance).
Artery undergoes small volume change (low compliance).
Functional corollaries
Arteries: pressure reservoir (elastic recoil sustains pressure).
Veins: volume reservoir (store extra blood without large pressure rise).
Boyle’s law underpinning elastic recoil effect: P \propto \frac{1}{V}
As aortic volume ↓ during recoil, pressure ↑ creating the diastolic “bump.”
Poiseuille’s law explaining resistance role of arterioles: Q = \frac{\Delta P}{R} \quad \text{with} \quad R \propto \frac{1}{r^4}
Tiny radius changes (via sphincter rings) produce huge resistance shifts.
Aortic stiffening (loss of elastic fibers with age or disease) ↓ compliance even further → widened pulse pressure & higher systolic load on LV.
Dysfunction of arteriolar control (e.g., sepsis → loss of tone; diabetes → microvascular disease) leads to tissue ischemia or edema.
Pharmacologic targets
Vasodilators (e.g., nitric-oxide donors) exploit metabolite pathways.
Calcium-channel blockers dampen myogenic constriction (used in hypertension, cerebral vasospasm).
Recognize structural differences among elastic, muscular, and arteriolar walls (tunica content).
Explain low compliance ➔ elastic recoil ➔ diastolic pressure maintenance.
Differentiate extrinsic vs intrinsic controls of arteriole tone (MAP vs tissue needs).
Outline metabolite vs myogenic mechanisms and identify tissues where each predominates.
Relate Poiseuille’s law to why arterioles are chief resistance vessels.
Apply concepts to clinical scenarios (aging arteries, kidney autoregulation, exercise hyperemia).