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Blood vessel
Diagram blood vessels
Details
SystemCirculatory system
Identifiers
Latinvas sanguineum
MeSHD001808
TA98A12.0.00.001
TA23895
FMA63183
Anatomical terminology

Blood vessels are the tubular structures of a circulatory system transporting blood in animal bodies.[1] Blood vessels transport blood cells, nutrients, and oxygen to most of the tissues of a body, and also transport waste products and carbon dioxide away from the tissues.[2] Some tissues – such as cartilage, epithelium, and the lens and cornea of the eye – are not supplied with blood vessels, so are termed avascular.

There are five types of blood vessels: the arteries, which carry the blood away from the heart; the arterioles; the capillaries, where the exchange of water and chemicals between the blood and tissues occurs; the venules; and the veins, which carry blood from the capillaries back towards the heart.

The word, vascular, is derived from the Latin vas, meaning vessel, and is used in reference to blood vessels.

Etymology

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  • artery – late Middle English; from Latin arteria, from Greek artēria, probably from airein ("raise").[3]
  • vein – Middle English; from Old French veine, from Latin vena.[4]
  • capillary – mid-17th century; from Latin capillaris, from capillus ("hair"), influenced by Old French capillaire.[5]

Structure

[edit]

The arteries and veins have three layers. The middle layer is thicker in the arteries than it is in the veins:[6]

  • The inner layer, tunica intima, is the thinnest layer. It is a single layer of flat cells (simple squamous epithelium) glued by a polysaccharide intercellular matrix, surrounded by a thin layer of subendothelial connective tissue interlaced with a number of circularly arranged elastic bands called the internal elastic lamina. A thin membrane of elastic fibers in the tunica intima run parallel to the vessel.
  • The middle layer of tunica media is the thickest layer in arteries. It consists of circularly arranged elastic fiber, connective tissue and polysaccharide substances; the second and third layer are separated by another thick elastic band called external elastic lamina.[7] The tunica media may (especially in arteries) be rich in vascular smooth muscle, which controls the caliber of the vessel. Veins do not have the external elastic lamina, but only an internal one. The tunica media is thicker in the arteries rather than the veins.
  • The outer layer is the tunica adventitia and the thickest layer in veins. It is entirely made of connective tissue. It also contains nerves that supply the vessel as well as nutrient capillaries (vasa vasorum) in the larger blood vessels.

Capillaries consist of a single layer of endothelial cells with a supporting subendothelium consisting of a basement membrane and connective tissue. When blood vessels connect to form a region of diffuse vascular supply, it is called an anastomosis. Anastomoses provide alternative routes for blood to flow through in case of blockages. Veins can have valves that prevent the backflow of the blood that was being pumped against gravity by the surrounding muscles.[8] In humans, arteries do not have valves except for the two 'arteries' that originate from the heart's ventricles.[9]

Early estimates by Danish physiologist August Krogh suggested that the total length of capillaries in human muscles could reach approximately 100,000 kilometres (62,000 mi) (assuming a high muscle mass human body, like that of a bodybuilder).[10] However, later studies suggest a more conservative figure of 9,000–19,000 kilometres (5,600–11,800 mi) taking into account updated capillary density and average muscle mass in adults.[11]

Types

[edit]

There are various kinds of blood vessels:[12]

They are roughly grouped as "arterial" and "venous", determined by whether the blood in it is flowing away from (arterial) or toward (venous) the heart. The term "arterial blood" is nevertheless used to indicate blood high in oxygen, although the pulmonary artery carries "venous blood" and blood flowing in the pulmonary vein is rich in oxygen. This is because they are carrying the blood to and from the lungs, respectively, to be oxygenated.[citation needed]

Function

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See also: Circulatory system

Blood vessels function to transport blood to an animal's body tissues. In general, arteries and arterioles transport oxygenated blood from the lungs to the body and its organs, and veins and venules transport deoxygenated blood from the body to the lungs. Blood vessels also circulate blood throughout the circulatory system. Oxygen (bound to hemoglobin in red blood cells) is the most critical nutrient carried by the blood. In all arteries apart from the pulmonary artery, hemoglobin is highly saturated (95–100%) with oxygen. In all veins, apart from the pulmonary vein, the saturation of hemoglobin is about 75%.[13][14] (The values are reversed in the pulmonary circulation.) In addition to carrying oxygen, blood also carries hormones, and nutrients to the cells of a body and removes waste products.[15]

Blood vessels do not actively engage in the transport of blood (they have no appreciable peristalsis). Blood is propelled through arteries and arterioles through pressure generated by the heartbeat.[16] Blood vessels also transport red blood cells. Hematocrit tests can be performed to calculate the proportion of red blood cells in the blood. Higher proportions result in conditions such as dehydration or heart disease, while lower proportions could lead to anemia and long-term blood loss.[17]

Permeability of the endothelium is pivotal in the release of nutrients to the tissue. It is also increased in inflammation in response to histamine,[18] prostaglandins[19] and interleukins,[20] which leads to most of the symptoms of inflammation (swelling, redness, warmth and pain).

Constriction

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Main article: Vasoconstriction
Transmission electron micrograph of a microvessel displaying an erythrocyte (E) within its lumen which is deformed due to vasoconstriction

Arteries—and veins to a degree—can regulate their inner diameter by contraction of the muscular layer. This changes the blood flow to downstream organs and is determined by the autonomic nervous system. Vasodilation and vasoconstriction are also used antagonistically as methods of thermoregulation.[21]

The size of blood vessels is different for each of them. It ranges from a diameter of about 30–25 millimeters for the aorta[22] to only about 5 micrometers (0,005 mm) for the capillaries.[23] Vasoconstriction is the constriction of blood vessels (narrowing, becoming smaller in cross-sectional area) by contracting the vascular smooth muscle in the vessel walls. It is regulated by vasoconstrictors (agents that cause vasoconstriction). These can include paracrine factors (e.g., prostaglandins), a number of hormones (e.g., vasopressin and angiotensin[24]) and neurotransmitters (e.g., epinephrine) from the nervous system.

Vasodilation is a similar process mediated by antagonistically acting mediators. The most prominent vasodilator is nitric oxide (termed endothelium-derived relaxing factor for this reason).[25]

Flow

[edit]
Main article: Vascular resistance

The circulatory system uses the channel of blood vessels to deliver blood to all parts of the body. This is a result of the left and right sides of the heart working together to allow blood to flow continuously to the lungs and other parts of the body. Oxygen-poor blood enters the right side of the heart through two large veins. Oxygen-rich blood from the lungs enters through the pulmonary veins on the left side of the heart into the aorta and then reaches the rest of the body. The capillaries are responsible for allowing the blood to receive oxygen through tiny air sacs in the lungs. This is also the site where carbon dioxide exits the blood. This all occurs in the lungs where blood is oxygenated.[26]

The blood pressure in blood vessels is traditionally expressed in millimetres of mercury (1 mmHg = 133 Pa). In the arterial system, this is usually around 120 mmHg systolic (high pressure wave due to contraction of the heart) and 80 mmHg diastolic (low pressure wave). In contrast, pressures in the venous system are constant and rarely exceed 10 mmHg.[27]

Vascular resistance occurs when the vessels away from the heart oppose the flow of blood. Resistance is an accumulation of three different factors: blood viscosity, blood vessel length and vessel radius.[28] Blood viscosity is the thickness of the blood and its resistance to flow as a result of the different components of the blood. Blood is 92% water by weight and the rest of blood is composed of protein, nutrients, electrolytes, wastes, and dissolved gases. Depending on the health of an individual, the blood viscosity can vary (i.e., anemia causing relatively lower concentrations of protein, high blood pressure an increase in dissolved salts or lipids, etc.).[28]

Vessel length is the total length of the vessel measured as the distance away from the heart. As the total length of the vessel increases, the total resistance as a result of friction will increase.[28] Vessel radius also affects the total resistance as a result of contact with the vessel wall. As the radius of the wall gets smaller, the proportion of the blood making contact with the wall will increase. The greater amount of contact with the wall will increase the total resistance against the blood flow.[29]

Disease

[edit]
Main article: Vascular disease

Blood vessels play a huge role in virtually every medical condition. Cancer, for example, cannot progress unless the tumor causes angiogenesis (formation of new blood vessels) to supply the malignant cells' metabolic demand.[30] Atherosclerosis represents around 85% of all deaths from cardiovascular diseases due to the buildup of plaque.[31] Coronary artery disease that often follows after atherosclerosis can cause heart attacks or cardiac arrest, resulting in 370,000 worldwide deaths in 2022.[32] In 2019, around 17.9 million people died from cardiovascular diseases. Of these deaths, around 85% of them were due to heart attack and stroke.[33]

Blood vessel permeability is increased in inflammation. Damage, due to trauma or spontaneously, may lead to hemorrhage due to mechanical damage to the vessel endothelium. In contrast, occlusion of the blood vessel by atherosclerotic plaque, an embolised blood clot or a foreign body leads to downstream ischemia (insufficient blood supply) and possibly infarction (necrosis due to lack of blood supply). Vessel occlusion tends to be a positive feedback system; an occluded vessel creates eddies in the normally laminar flow or plug flow blood currents. These eddies create abnormal fluid velocity gradients which push blood elements, such as cholesterol or chylomicron bodies, to the endothelium. These deposit onto the arterial walls which are already partially occluded and build upon the blockage.[34]

The most common disease of the blood vessels is hypertension or high blood pressure. This is caused by an increase in the pressure of the blood flowing through the vessels. Hypertension can lead to heart failure and stroke. Aspirin helps prevent blood clots and can also help limit inflammation.[35] Vasculitis is inflammation of the vessel wall due to autoimmune disease or infection.


References

[edit]
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Blood vessel

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from Grokipedia
Blood vessels are the tubular structures that constitute the vascular system, forming a closed network of conduits that transport throughout the body, delivering oxygen and nutrients to tissues while removing and metabolic wastes. They form part of the alongside the heart and , enabling the distribution of essential substances and the maintenance of . Blood vessels are classified into three main types based on their structure and function: arteries, which generally carry oxygenated blood away from the heart under high pressure (except the pulmonary arteries, which carry deoxygenated blood); veins, which generally return deoxygenated blood to the heart under lower pressure and often contain one-way valves to prevent backflow (except the pulmonary veins, which carry oxygenated blood); and capillaries, the smallest vessels that facilitate the exchange of gases, nutrients, and wastes between blood and tissues via diffusion. Arteries and veins further branch into smaller arterioles and venules, respectively, which help regulate blood flow to specific organs and tissues. Structurally, most blood vessels consist of three layers: the , an inner endothelial lining that provides a smooth surface for blood flow; the tunica media, a middle layer of and elastic tissue that controls vessel diameter and ; and the , an outer layer that anchors the vessel. Capillaries, however, have only a single endothelial layer to maximize permeability for exchange processes. These layered walls adapt to the vessels' roles, with arteries featuring thicker, more elastic media to withstand pulsatile pressure, while veins are thinner and more compliant to accommodate larger blood volumes. In addition to transport, blood vessels play critical roles in thermoregulation by dilating or constricting to adjust blood flow to the skin, and in hemostasis by constricting upon injury to minimize blood loss. The vascular system's integrity is vital for overall health, as dysfunction can lead to conditions like or , underscoring its foundational importance in human physiology.

Structure

Layers of the Vessel Wall

Blood vessel walls are composed of three primary histological layers, known as tunicae, which provide structural support, regulate blood flow, and facilitate interaction with surrounding tissues. The innermost layer, the , consists of a continuous of endothelial cells forming a that lines the vessel lumen, overlaid by a thin subendothelial layer of containing and elastic fibers. This serves as a selective barrier, preventing through anticoagulant mechanisms such as the production of and , which inhibit platelet aggregation and promote . Additionally, it regulates by controlling the paracellular transport of solutes and macromolecules between the bloodstream and interstitial space. The middle layer, the tunica media, is primarily composed of circumferentially arranged cells interspersed with elastic fibers, which allow for vessel contraction and elasticity to accommodate pressure changes. In larger arteries, this layer is notably thick and rich in elastic components to withstand and recoil from pulsatile blood flow. The outermost layer, the tunica adventitia, comprises dominated by fibers, with some and fibroblasts, anchoring the vessel to surrounding structures and providing tensile strength. The relative thickness and composition of these layers vary across vessel types to suit their hemodynamic demands; for instance, arteries feature a thicker tunica media compared to veins, which have a more prominent . In larger vessels, where from the lumen is insufficient, the —a network of microvessels within the tunica adventitia and outer media—supply oxygen and nutrients to the wall cells while removing waste products.

Arteries

Arteries are muscular, tubular structures that transport blood away from the heart to the body's tissues, carrying oxygenated blood in the systemic circulation (with the exception of the pulmonary arteries, which carry deoxygenated blood). They operate under high pressure generated by ventricular contraction. Unlike veins, arteries feature thick walls adapted to withstand pulsatile flow without collapsing, ensuring efficient distribution to peripheral regions. In the arterial system, blood pressure peaks during systole at approximately 120 mmHg, necessitating robust structural reinforcements to prevent vessel rupture or dilation. Arteries are classified into two primary types based on their location and composition: elastic arteries and muscular arteries. Elastic arteries, such as the aorta and pulmonary artery, are the largest vessels closest to the heart and contain abundant elastin fibers in the tunica media, allowing them to stretch during systole and recoil during diastole to maintain steady blood flow. Muscular arteries, exemplified by the femoral artery, predominate in the periphery and possess a thicker layer of smooth muscle cells relative to elastic fibers in the tunica media, enabling precise vasoregulation in response to local metabolic demands. This classification reflects adaptations for conducting high-volume blood from the heart versus distributing it to specific organs. The structural adaptations of arteries center on a prominent tunica media, which comprises alternating layers of and elastic lamellae—concentric sheets of that provide resilience against cyclic pressure. These features result in relatively narrow lumens compared to veins of similar caliber, optimizing resistance to high-pressure flow while minimizing energy loss. The , the principal elastic artery, measures about 2.5 cm in diameter at its root, progressively branching into smaller arteries and eventually arterioles that feed capillary beds. Arteries lack valves, relying instead on their elastic properties and continuous forward propulsion from the heart to prevent backflow. Recent estimates of the human capillary network, totaling 9,000–19,000 km in length, underscore the extensive branching of arterial trees required to perfuse such a vast exchange surface, influencing the density and distribution of arterial vessels throughout tissues.

Veins

Veins are blood vessels that conduct blood from tissues back to the heart, carrying deoxygenated blood in the systemic circulation (with the exception of the pulmonary veins, which carry oxygenated blood). They function as the low-pressure counterparts to arteries in the circulatory system. Their structure is adapted for handling lower pressures and serving as a reservoir for blood volume, with walls that are generally thinner and more compliant than those of arteries. The venous wall comprises three primary layers: the innermost , a thin middle tunica media, and an outer . In medium and large veins, the tunica media is notably thinner than in corresponding arteries, featuring only a few layers of cells and elastic fibers, which limits its role in active contraction. Conversely, the is the thickest layer, composed mainly of and elastic fibers that provide structural support and help prevent vessel collapse under low internal pressure. To ensure unidirectional flow despite this low pressure, medium and large veins (typically those greater than 2 mm in diameter) incorporate one-way valves formed by bicuspid folds of the endothelium, which close to block retrograde blood movement. Veins are broadly classified into superficial and deep categories based on their anatomical location and role in circulation. Superficial veins lie in the subcutaneous tissue just beneath the skin, draining blood from cutaneous structures and often visible or palpable. Deep veins, embedded within muscles and accompanied by arteries, form the primary conduits for returning blood from deeper tissues to the heart. Connecting these systems are perforator veins, which penetrate the muscular fascia to link superficial and deep networks, facilitating blood transfer primarily from superficial to deep veins under normal conditions. The largest veins in the body are the superior and inferior venae cavae, with the inferior vena cava exhibiting a mean diameter of approximately 2 cm (ranging from 1.3 to 3 cm in adults). Veins accommodate roughly 60-70% of the total circulating at rest, acting as a major that can mobilize as needed for . This is enabled by their low intraluminal , which is typically under 10-15 mmHg in peripheral veins and 8-12 mmHg centrally, far below arterial levels. The flaccid nature of venous walls, with high compliance due to abundant elastic and collagenous tissue, allows veins to distend and store variable volumes of without significant pressure changes, thereby buffering circulatory demands.

Capillaries

Capillaries are the smallest vessels in the , typically measuring 5 to 10 micrometers in , which is comparable to the of a , allowing for efficient passage of cells through these narrow conduits. They consist of a single layer of endothelial cells surrounded by a thin , with occasional providing structural support, but lack cells found in larger vessels. This minimalist structure facilitates the primary function of capillaries: the exchange of oxygen, nutrients, , and waste products between and surrounding tissues via . Capillaries form extensive networks that connect arterioles to venules, creating a vast interface for molecular transport. Capillaries are classified into three main types based on their endothelial structure and permeability, which adapt to the specific needs of different tissues. Continuous capillaries feature a complete endothelial lining with tight junctions, minimizing leakage and providing a selective barrier; they predominate in muscles, , and the . Fenestrated capillaries have endothelial cells perforated by small pores (fenestrae) of about 70-100 nanometers, enhancing filtration and absorption; these are common in the kidneys (for glomerular filtration) and endocrine glands. Sinusoidal capillaries, also known as discontinuous capillaries, possess larger gaps (up to 100 micrometers) between endothelial cells and an incomplete , allowing passage of larger molecules and cells; they occur in the liver, , and to support high-volume exchange. In the , the total length of is estimated at 9,000 to 19,000 kilometers, a revised figure from earlier calculations of around 100,000 kilometers proposed by in 1922, which was based on overstated muscle mass and capillary density assumptions. The total surface area of these capillaries is approximately 500 to 1,000 square meters, providing an immense area for exchange equivalent to several football fields. Unlike arteries and veins, capillaries contain no , relying instead on precapillary sphincters in arterioles for flow regulation. The density of capillary networks varies significantly across tissues, reflecting metabolic demands; for instance, the lungs exhibit exceptionally high capillary density, with an extensive mesh surrounding alveoli to maximize efficiency. In contrast, tissues like have moderate densities (around 300 capillaries per square millimeter), while the maintains a dense network to support high oxygen needs without compromising the blood-brain barrier.

Function

Blood Flow and Circulation

Blood flow through the vascular system follows two primary circulatory pathways: the systemic circulation and the pulmonary circulation. In systemic circulation, oxygenated blood is pumped from the left ventricle of the heart through the aorta and into arteries, distributing it to body tissues for nutrient and oxygen delivery before returning deoxygenated blood via veins to the right atrium. Conversely, pulmonary circulation carries deoxygenated blood from the right ventricle through the pulmonary arteries to the lungs for gas exchange, where it becomes oxygenated and returns via pulmonary veins to the left atrium. These pathways operate in series, ensuring continuous blood circulation driven by the heart's pumping action, with the systemic circuit handling higher pressures to overcome greater resistance in the body's extensive vascular network. The principles governing blood flow are rooted in , particularly Poiseuille's law, which describes the resistance to in cylindrical vessels. According to Poiseuille's law, flow resistance RR is given by R=8ηLπr4R = \frac{8 \eta L}{\pi r^4}, where η\eta is , LL is vessel length, and rr is , demonstrating that resistance is inversely proportional to the of the radius (R∝1r4R \propto \frac{1}{r^4}). This relationship explains why small changes in vessel radius profoundly affect flow rates, with total averaging approximately 5 L/min in a resting , distributed across the vascular . Blood velocity varies inversely with cross-sectional area: it is highest in large arteries at about 50 cm/s, slows dramatically to 0.03 cm/s in capillaries to facilitate exchange, and averages 20 cm/s in veins. gradients drive this flow, with arterial pressures typically 120/80 mmHg (systolic/diastolic) and venous pressures ranging from about 15 mmHg peripherally to near 0 mmHg centrally. reflects these pathways, at 95–100% in and around 75% in mixed . Blood flow is predominantly laminar in most vessels but can become turbulent under certain conditions, determined by the (Re=ρvDηRe = \frac{\rho v D}{\eta}, where ρ\rho is , vv is , DD is , and η\eta is ). A exceeding 2,000 in large vessels indicates the onset of turbulence, potentially increasing loss and on vessel walls, though normal physiological flows remain mostly laminar to minimize such disruptions. This transition is rare in healthy circulation but can occur at vessel bifurcations or during high-flow states like exercise.

Vascular Regulation

Vascular regulation encompasses the dynamic processes that adjust diameter to control blood distribution, pressure, and flow throughout the body. These mechanisms primarily involve , which narrows vessels to increase resistance and redirect blood, and , which widens vessels to decrease resistance and enhance . Regulation occurs through neural, hormonal, local metabolic, and intrinsic vascular responses, enabling precise adaptation to physiological demands such as exercise or rest. Neural control is predominantly mediated by the , which releases norepinephrine to induce via activation of alpha-1 adrenergic receptors on vascular cells in arteries and arterioles. In contrast, parasympathetic influences and activation promote , particularly in beds during sympathetic activation. Hormonal regulation includes II, a key component of the renin-angiotensin system, which binds to AT1 receptors on vascular to cause potent , thereby supporting maintenance. Local metabolic factors, such as elevated (CO₂) levels and reduced oxygen, trigger in response to tissue hypoxia or , ensuring increased blood supply to active regions. Endothelial cells play a central role in vascular tone by releasing paracrine factors; (NO), produced by endothelial (eNOS), diffuses to cells to activate , increasing cyclic GMP and inducing relaxation for . Conversely, endothelin-1, secreted by endothelial cells under stress, binds to ET_A receptors on to promote constriction via calcium influx. The myogenic response in arterioles involves intrinsic contraction in response to increased intraluminal , where stretch activates mechanosensitive ion channels, leading to and calcium entry to sustain tone and protect downstream capillaries from surges. Autoregulation maintains relatively constant blood flow despite fluctuations in perfusion , primarily through myogenic mechanisms in organs like the and kidneys. In the , autoregulation integrates myogenic constriction, neurogenic influences from perivascular nerves, endothelial NO release, and metabolic signals like to stabilize flow between mean arterial pressures of 60-160 mmHg. Renal autoregulation similarly relies on myogenic responses in and to preserve amid pressure changes. Flow-mediated dilation represents a key adaptive mechanism where increased shear stress on the endothelium, due to elevated blood flow, stimulates eNOS activation and NO production, leading to rapid vasodilation in conduit arteries like the brachial. This process, observed in healthy vessels, underscores the endothelium's role in matching vessel caliber to hemodynamic demands and has been linked to cardiovascular health in clinical assessments.

Exchange Processes

Blood vessels, particularly capillaries, serve as the primary sites for the exchange of nutrients, gases, and waste products between the bloodstream and surrounding tissues. This process ensures that oxygen and nutrients reach cells while and metabolic wastes are removed, maintaining tissue . Exchange occurs across the thin endothelial walls of capillaries, which are optimized for permeability while preventing excessive fluid loss. Diffusion is the principal mechanism for the transport of small molecules such as oxygen (O₂), (CO₂), and glucose across walls. According to Fick's first law of , the (J) of a substance is proportional to the concentration (ΔC), surface area (A), and inversely proportional to the thickness (Δx): J∝A⋅ΔCΔxJ \propto \frac{A \cdot \Delta C}{\Delta x} This law explains why capillaries have thin walls (approximately 0.5–1 μm thick) and extensive surface area (approximately 500–1,000 m² in humans) to maximize exchange rates. For instance, O₂ diffuses from blood ( ~100 mmHg in arteries) to tissues (~40 mmHg), while CO₂ moves in the opposite direction due to its steeper . Glucose, with a concentration from plasma (~5 mM) to interstitial fluid (~4 mM), follows similarly, supporting cellular energy needs. In addition to diffusion, fluid exchange between capillaries and tissues is governed by filtration and osmosis, driven by Starling forces that balance hydrostatic and oncotic pressures. Hydrostatic pressure (from blood flow) pushes fluid out at the arterial end of the capillary (typically ~30–35 mmHg), while oncotic pressure (from plasma proteins, ~25 mmHg) pulls fluid back in at the venous end (~15 mmHg). The net filtration pressure is approximately 10 mmHg outward at the arterial end, favoring filtration into the interstitium, and reverses to reabsorption at the venous end, ensuring fluid balance. This dynamic prevents edema by recycling about 20 liters of fluid daily back into circulation. Capillary permeability varies by solute size and type, with high permeability coefficients for (enabling rapid flux) and low for proteins (reflection coefficient near 1, restricting passage to <1% of plasma levels). Fenestrated capillaries, such as those in the kidneys, feature pores that further enhance and small solute exchange. Excess filtered and escaped proteins are drained by lymphatic vessels, which absorb at rates up to 2–4 liters per day, returning it to the venous system via the . In specialized tissues, exchange is tightly regulated; for example, the blood-brain barrier consists of continuous with tight junctions that limit permeability to essential nutrients while excluding toxins and large molecules. This structure maintains the brain's unique microenvironment, with permeability coefficients for high but for proteins and ions extremely low.

Development

Embryonic Formation

The formation of blood vessels in the embryo begins with vasculogenesis, a de novo process where angioblasts—derived from mesodermal precursors in the lateral plate mesoderm—differentiate into endothelial cells and assemble into primitive vascular tubes. This initial vascular network emerges primarily in extraembryonic structures, such as the yolk sac, around the third week of human gestation, establishing the foundational plexus for blood circulation. In parallel, the heart tube forms from cardiogenic mesoderm and begins beating by embryonic day 21, initiating primitive blood flow through these early vessels. Vasculogenesis proceeds through the migration and coalescence of angioblasts, guided by gradients of signaling molecules that promote their specification and organization into cords that lumenize into tubes. Key molecular signals include (FGF), which induces mesodermal cells toward the angioblast lineage, and transforming growth factor-β (TGF-β), which supports endothelial differentiation while inhibiting excessive proliferation to stabilize nascent structures. (VEGF), secreted by surrounding endodermal cells, further drives angioblast proliferation and migration via its receptor VEGFR2 (Flk-1), establishing a cranial-to-caudal and dorsal-to-ventral patterning of the primitive vascular bed. Following vasculogenesis, angiogenesis expands the vascular network through sprouting and branching from existing vessels, particularly in the yolk sac and chorion by week 3, where VEGF plays a central role in stimulating endothelial cell proliferation, migration, and tube extension. This process refines the initial plexus into a hierarchical system, with paired dorsal aortae forming along the embryonic axis and fusing caudally to create the descending aorta. Concurrently, six pairs of aortic arches develop within the branchial (pharyngeal) arches from the aortic sac, connecting the ventral outflow to the dorsal aortae and laying the groundwork for major arterial trunks. These embryonic vessels serve as precursors to adult arteries and veins, with early molecular cues like differential VEGF signaling beginning to specify arterial versus venous identities.

Postnatal Maturation

Postnatal maturation of blood vessels involves adaptive changes that support the transition from fetal to independent circulation and accommodate growth, hormonal influences, and aging. At birth, lung expansion with the first breath mechanically dilates pulmonary vessels, leading to a rapid tenfold increase in pulmonary blood flow and a decrease in pulmonary vascular resistance to less than 5% of fetal levels, primarily driven by rising oxygen tension. Concurrently, fetal shunts such as the ductus arteriosus undergo functional closure through oxygen-induced smooth muscle constriction, followed by anatomic remodeling involving intimal proliferation and fibrosis, ensuring separation of systemic and pulmonary circulations. The foramen ovale typically closes functionally within hours due to left atrial pressure exceeding right atrial pressure, with anatomic fusion occurring over weeks. As tissues grow postnatally, hypoxia in expanding organs triggers neovascularization via , where hypoxia-inducible factor-1 (HIF-1) upregulates (VEGF), promoting endothelial cell proliferation and new vessel formation to meet metabolic demands. This process is evident in developing and , where localized hypoxia from rapid growth stimulates capillary sprouting and network expansion. Conversely, unused vessels regress; for instance, the fully remodels and obliterates within 2-3 weeks if not pathologically patent, through and changes, preventing inefficient shunting. Hormonal and environmental factors further shape vascular maturation. In females, enhances arterial elasticity by stimulating endothelial , promoting and reducing vessel stiffness, particularly during reproductive years. Exercise training induces capillary growth in skeletal muscles, increasing density by up to 23% and the capillary-to-fiber ratio through shear stress-mediated VEGF expression, thereby improving oxygen capacity. Aging progressively alters vascular structure and function, with large elastic arteries stiffening due to fragmentation, accumulation, and cross-linking, which more than doubles aortic stiffness over a lifetime and elevates systolic . Endothelial function declines with age through reduced bioavailability and increased , impairing and heightening risk, independent of other factors.

Pathology

Common Vascular Diseases

Common vascular diseases encompass a range of conditions that impair blood vessel integrity and function, contributing significantly to global morbidity and mortality. Cardiovascular diseases (CVDs), many of which stem from vascular pathologies, accounted for 17.9 million deaths worldwide in 2019, with approximately 85% of these due to heart attacks and strokes. In 2022, —a key vascular disorder—resulted in 371,506 deaths in the United States alone. These diseases often arise from disruptions in vessel wall , such as endothelial damage in the intima layer, which exposes subendothelial tissues and initiates pathological cascades. Atherosclerosis is a primary characterized by the buildup of plaques in arterial walls, leading to luminal and reduced blood flow. The process begins with endothelial activation and dysfunction, followed by the accumulation of , fibrous elements, and within the intima. (LDL) oxidation plays a critical role, as oxidized LDL promotes recruitment, formation, and chronic , exacerbating plaque progression and instability. Advanced plaques can rupture, triggering acute events like or ischemic stroke. Aneurysms involve localized weakening and dilation of blood vessel walls, increasing the risk of rupture and life-threatening hemorrhage. In abdominal aortic aneurysms (AAAs), the most common type, degradation of and in the media layer, often driven by and proteolytic enzymes, compromises structural integrity. Hypertension accelerates this process by imposing chronic mechanical stress on the vessel wall, elevating rupture risk, which rises exponentially with aneurysm diameter exceeding 5 cm. Thrombosis refers to the pathological formation of blood clots within vessels, obstructing flow and potentially causing ischemia or . It arises from : endothelial injury, blood flow stasis or turbulence, and hypercoagulability, where activated platelets and factors aggregate on damaged surfaces. Arterial thrombosis often complicates , while venous thrombosis, such as deep vein thrombosis, frequently occurs in the lower extremities due to immobility or hypercoagulable states. Vasculitis encompasses inflammatory disorders of blood vessels, leading to wall thickening, , and organ ischemia. involves immune-mediated damage, including deposition and infiltration, which erode the and . , affecting medium and large arteries, exemplifies this through granulomatous inflammation, commonly impacting the temporal artery and risking vision loss if untreated. Peripheral artery disease (PAD) manifests as primarily in the lower extremity arteries, causing and tissue ischemia. Narrowing of the iliac, femoral, or popliteal arteries reduces , with plaque formation mirroring coronary but often progressing asymptomatically until critical limb ischemia develops. Risk factors like smoking and amplify , leading to widespread vascular occlusion.

Risk Factors and Prevention

Risk factors for vascular diseases are categorized into non-modifiable and modifiable types, influencing the development of conditions such as and (PAD). Non-modifiable risk factors include advanced age, which is strongly associated with the presence and progression of vascular damage, as endothelial function declines with aging. Male sex also heightens susceptibility, with studies showing a significant link to increased vascular damage extent compared to females. , often manifested as family history of (CVD), further elevates risk independently of other factors. Modifiable risk factors encompass and health conditions that can be addressed to mitigate vascular harm. is a prominent example, as current smokers face more than twice the risk of premature atherosclerotic CVD compared to never-smokers, primarily through endothelial injury and accelerated plaque formation. damages vessel walls, promoting ; impairs endothelial function via ; contributes to plaque buildup from excess ; and a fosters and reduced vascular compliance. Emerging evidence from 2022 highlights , particularly fine particulate matter (PM2.5), as a modifiable environmental inducing and , with meta-analyses linking short- and long-term exposure to heightened CVD morbidity. Prevention strategies emphasize lifestyle modifications and pharmacological interventions to target these modifiable risks and preserve vascular health. A , rich in fruits, vegetables, whole grains, and healthy fats while low in saturated fats, reduces CVD risk by approximately 30%, as demonstrated in high-risk populations through improved lipid profiles and anti-inflammatory effects. Regular exercise enhances endothelial function by promoting and reducing , with guidelines recommending at least 150 minutes of moderate aerobic activity weekly to lower and obesity-related risks. Pharmacologically, statins are first-line for managing in primary prevention, effectively lowering cholesterol and atherosclerotic progression in those with elevated levels. Antihypertensive agents, such as ACE inhibitors or beta-blockers, mitigate vessel strain and reduce CVD events when exceeds 130/80 mmHg. Screening plays a key role in early detection and prevention, particularly for PAD. The ankle-brachial index (ABI), a non-invasive test comparing arm and ankle blood pressures, is recommended for asymptomatic adults over 65 or those with risk factors like or ; an ABI below 0.90 indicates PAD and prompts intervention to prevent progression. Overall, addressing modifiable factors through combined lifestyle and medical approaches can substantially decrease incidence.

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK470401/
  2. https://pressbooks.uwf.edu/medicalterminology/chapter/blood-vessels-and-blood/
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