Smooth muscle and the cardiovascular and lymphatic systems

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CHAPTER 6 Smooth muscle and the cardiovascular and lymphatic systems

The cardiovascular system carries blood from the heart to all parts of the body through a series of tubes, all but the smallest of which are muscular. The muscle in these tubes is of two types: smooth muscle is characteristic of the walls of blood vessels and cardiac muscle provides the walls of the heart chambers with their powerful contractile pumping action. The general characteristics and classification of muscle tissues are given on page 103. Smooth muscle also forms an important contractile element in the walls of many other organ systems of the body, e.g. the gastrointestinal tract.


In smooth muscle tissue the contractile proteins actin and myosin are not organized into regular sarcomeres, visible as transverse striations, so the cytoplasm has a smooth (unstriated) appearance. Smooth muscle is also referred to as involuntary muscle, because its activity is neither initiated nor monitored consciously. It is more variable, in both form and function, than either striated or cardiac muscle, a reflection of its varied roles in different systems of the body.

Smooth muscle cells (fibres) are smaller than those of striated muscle. Their length can range from 15 μm in small blood vessels to 200 μm, and even to 500 μm or more in the uterus during pregnancy. The cells are spindle-shaped, tapering towards the ends from a central diameter of 3–8 μm (Fig. 6.1). The nucleus is single, located at the midpoint, and often twisted into a corkscrew shape by the contraction of the cell. Smooth muscle cells aggregate with their long axes parallel and staggered longitudinally, so that the wide central portion of one cell lies next to the tapered end of another. Such an arrangement achieves both close packing and a more efficient transfer of force from cell to cell. In transverse section, smooth muscle is seen as an array of circular or slightly polygonal profiles of very varied size, and nuclei are present only in the centres of the largest profiles (Fig. 6.2). This appearance contrasts markedly with that of skeletal muscle cells, which show a consistent diameter in cross-section and peripherally placed nuclei throughout their length.

Smooth muscle is typically found in the walls of tubular structures and hollow viscera. It regulates diameter (e.g. in blood vessels, and branches of the bronchial tree); propels liquids or solids (e.g. in the ureter, hepatic duct, and intestines); or expels the contents (e.g. in the urinary bladder and uterus). The actual arrangement of the cells varies with the tissue. The account that follows will therefore be concerned with the generic properties of smooth muscle. The more specialized morphologies of smooth muscle are described in the appropriate regional chapters.

Smooth muscle has no attachment structures equivalent to the fasciae, tendons and aponeuroses associated with skeletal muscle. There is a special arrangement for transmitting force from cell to cell and, where necessary, to other soft tissue structures. Cells are separated by a gap of 40–80 nm. Each cell is covered almost entirely by a prominent basal lamina which merges with a reticular layer consisting of a network of fine elastin, reticular fibres (collagen type III) and type I collagen fibres (Fig. 6.3). These elements bridge the gaps between adjacent cells and provide mechanical continuity throughout the fascicle. The cell attaches to components of this extracellular matrix at dense plaques (see Fig. 6.4A) where the basal lamina is thickened; cell–cell attachment occurs at intermediate junctions or desmosomes, formed of two adjacent dense plaques. At the boundaries of fascicles, the connective tissue fibres become interwoven with those of interfascicular septa, so that the contraction of different fascicles is communicated throughout the tissue and to neighbouring structures. The components of the reticular network, the ground substance and collagen and elastic fibres, are synthesized by the smooth muscle cells themselves, not by fibroblasts or other connective tissue cells, which are rarely found within fasciculi.

In some blood vessels, notably those of the pulmonary circulation, and in the airways, and probably in other smooth muscle types, there is evidence for heterogeneity of cell phenotype. Some myofibroblast-like cells have a function that is more secretory than contractile. The secretory phenotype is often increased in disease (e.g. chronic severe asthma, pulmonary hypertension) and is associated with increased proliferation and remodeling, also the secretion of cytokines and other mediators. Many smooth muscles seem to exhibit considerable plasticity between these contractile and secretory phenotypes.

Discontinuities occur in the basal lamina between adjacent cells, and here the cell membranes approach to 2–4 nm of one another to form a gap junction (Fig. 6.2). These junctions are believed to be structurally similar to their counterparts in cardiac muscle. They provide a low-resistance pathway through which electrical excitation can pass between cells, producing a coordinated wave of contraction. The incidence of gap junctions varies with the anatomical site of the tissue: they appear to be more abundant in the type of smooth muscle which generates rhythmic (phasic) activity.

Although some smooth muscles can generate as much force per unit cross-sectional area as skeletal muscle, the force always develops much more slowly than in striated muscle. Smooth muscle can contract by more than 80%, a much greater range of shortening than the 30% or so to which striated muscle is limited. The significance of this property is illustrated by the urinary bladder, which is capable of emptying completely from an internal volume of 300 ml or more. Smooth muscles can maintain tension for long periods with very little expenditure of energy. Many smooth muscle structures are able to generate spontaneous contractions: examples are found in the walls of the intestines, ureter and uterine tube.


Although electron microscopy revealed the presence of filaments in smooth muscle some years ago, this observation alone provided little insight into their mode of function because of the lack of any obvious organization of the filaments. More recent work, using high-resolution immunocytochemistry, has revealed further details of the internal architecture of the cell and suggests a structural basis for contractile function. The model, which is illustrated in Fig. 6.3, depends on the mutual interaction of two systems of filaments, one forming the cytoskeleton and the other the contractile apparatus.

Excluding the perinuclear region, the cytoplasm of a smooth muscle cell effectively consists of two structural domains. The cytoskeleton forms a structural framework that maintains the spindle-like form of the cell and provides an internal scaffold with which other elements can interact. Its major structural component is the intermediate filament desmin, with the addition of vimentin (which may also be present alone) in vascular smooth muscle. The intermediate filaments are arranged mainly in longitudinal bundles, but some filaments interconnect the bundles with each other and with the sarcolemma to form a three-dimensional network. The bundles of intermediate filaments insert into focal, electron-dense bodies, approximately 0.1 μm in diameter, which are distributed uniformly throughout the cytoplasm and also attach to dense plaques underlying the plasma membrane (Fig. 6.3A). The cytoplasmic dense bodies and submembraneous dense plaques are equivalent to the Z-discs of striated muscle cells. They contain the actin-binding protein α-actinin and thus also anchor the actin filaments of the contractile apparatus. These form a lattice of obliquely arranged bundles throughout the cytoplasm, which transmit force to the plasma membrane and thus the basal lamina and extracellular matrix via dense plaques. These are associated with a highly structured arrangement of ancillary proteins, including vinculin and talin, which in turn attach to integrins that cross the membrane and provide attachment to components of the extracellular matrix. An analogous arrangement underlies cell–cell attachment at desmosomes, but here the attachment between dense plaques is provided by transmembrane cadherin glycoproteins and intracellular catenins instead of integrins and talin. Mechanical deformation of the cell may be linked to cell signalling mechanisms via focal adhesion kinase (FAK) and its substrate paxillin; phosphorylation of talin and paxillin may modulate the deformability of the smooth muscle cell. Other regulatory proteins also associate specifically with actin, such as caldesmon and calponin. The cytoskeleton is therefore not a passive structure, and can adapt dynamically to load, presumably therefore contributing to the low energy requirements of smooth muscle contraction. The ratio of actin to myosin is about eight times greater in smooth compared to striated muscle, reflecting the greater length of actin filaments in smooth muscle.

Smooth muscle myosin filaments are 1.5–2 μm long, somewhat longer than those of striated muscle. Although smooth muscle cells contain less myosin, the longer filaments are capable of generating considerable force. The myosin filaments of smooth muscle are also assembled differently, such that their head regions lie symmetrically on either side of a ribbon-like filament, rather than imposing a bipolar organization on the filament. Actin filaments, to which they bind, can thus slide along the whole length of the myosin filament during contraction. This difference underpins the ability of smooth muscle to undergo much greater changes in length than striated muscle. Actin–myosin filament sliding generates tension which transmits to focal regions of the plasma membrane, changing the cell to a shorter, more rounded shape (Fig. 6.3B) and often deforming the nucleus to a corkscrew-like profile.

Caveolae, cup-like invaginations of the plasma membrane with a resemblance to endocytotic vesicles, are a characteristic feature of smooth muscle cells, and may form up to 30% of the membrane (Fig. 6.4). They are associated with many receptors, ion channels and kinases, and the peripheral sarcoplasmic reticulum and may thus act as sites for highly localized signalling pathways. They may also act as specialized pinocytotic structures involved in fluid and electrolyte transport into the cell. Other organelles (mitochondria, ribosomes etc) are largely confined to the filament-free perinuclear cytoplasm, although in some smooth muscle types, including vascular smooth muscle, peripheral mitochondria, sarcoplasmic reticulum and sarcolemma seem to form signalling microdomains. Recent studies using mitochondria-specific staining of such smooth muscle cells often show mitochondria forming a reticular network within the cytosol, which would be consistent with a cell signalling function, especially that concerned with intracellular calcium homeostasis.


Smooth muscle may contract in response to nervous or hormonal stimulation, or electrical depolarization transferred from neighbouring cells. Some muscles receive a dense innervation to all cells; these are often referred to as multi-unit smooth muscles, and most blood vessels are of this type. Such innervation can precisely define contractile activity, e.g. in the iris, specific nervous control can produce either pupillary constriction or dilation. Other muscles are more sparsely innervated. They tend to display myogenic activity, initiated spontaneously or in response to stretch, which may be markedly influenced by hormones. In these muscles, which include those in the walls of the gastrointestinal tract, urinary bladder, ureter, uterus and uterine tube, innervation tends to exert a more global influence on the rate and force of intrinsically generated contractions. These muscles have been referred to as unitary smooth muscles. The terms multi-unit and unitary smooth muscles are widely used, but in practice such distinctions are better regarded as the extremes of a continuous spectrum.

Smooth muscles are innervated by unmyelinated axons whose cell bodies are located in autonomic ganglia, either in the sympathetic chain or, in the case of parasympathetic fibres, closer to the point of innervation (Fig. 6.5). They ramify extensively, spreading over a large area of the muscle and sending branches into the muscle fasciculi. The terminal portion of each axonal branch is beaded, and consists of expanded portions, varicosities, packed with vesicles and mitochondria, separated by thin, intervaricose portions. Each varicosity is regarded as a transmitter release site, and, in the functional sense, is therefore a nerve ending. In this way the axonal arborization of a single autonomic neurone bears a very large number of nerve endings (up to tens of thousands), as opposed to a maximum of a few hundred in somatic motor neurones. The neuromuscular terminals of autonomic efferents are considered in more detail on page 62.

The neuromuscular junctions in smooth muscles do not show the consistent appearance seen in skeletal muscles. The neurotransmitter diffuses across a gap that can vary from 10 to 100 nm: even separations up to 1 μm may still allow neuromuscular transmission to take place, although more slowly. The nerve ending is packed with vesicles, but the adjacent area of the muscle cell is not structurally differentiated from that of non-junctional regions – there is no distinct synapse.

Intramuscular afferent nerves are the peripheral processes of small sensory neurones in the dorsal root ganglia. Since they are unmyelinated, contain axonal vesicles and have a beaded appearance, they are difficult to distinguish from efferent fibres, except by differential staining for neurotransmitters.


Excitation–contraction coupling in smooth muscle may be electromechanical or pharmacomechanical. Electromechanical coupling involves depolarization of the cell membrane by an action potential, and may be generated when a membrane receptor, usually linked with an ion channel, is occupied by a neurotransmitter, hormone or other blood-borne substance. It is most commonly seen in unitary smooth muscles such as those of the viscera, with transmission of electrical excitation from cell to cell via gap junctions. In some types of smooth muscle, depolarization may be the consequence of other stimuli, such as cooling, stretching, and even light.

Pharmacomechanical coupling is a receptor-mediated and G-protein coupled process, which can activate constriction via several pathways. These include triggering the formation of inositol trisphosphate, which acts as a signal for intracellular calcium release from the sarcoplasmic reticulum, activation of voltage-independent calcium channels in the sarcolemma, and depolarization causing activation of voltage-dependent calcium channels. In addition, some receptors couple to kinases that modulate contraction in a calcium independent fashion, either via myosin phosphatase (see below), or via the actin cytoskeleton. Different types of smooth muscle use these pathways to differing extents.

The regulation of contraction of smooth muscle is however largely calcium-dependent. In the cytoplasm, calcium binds to calmodulin. The complex so formed regulates the activity of myosin light chain kinase, which phosphorylates myosin regulatory light chains and initiates the myosin-actin ATPase cycle (p. 111). The enzymatic activation process is therefore inherently slow. Unphosphorylated myosin II of smooth muscle cannot initiate actin binding, although it can maintain contraction, with little energy expenditure. Myosin phosphatase dephosphorylates myosin light chains, and thus promotes relaxation. Inhibition of the phosphatase, for example by Rho kinase, increases phosphorylation for any level of calcium (i.e. increases calcium sensitivity). This is now believed to be a very important component of the response to many constrictor agonists.


It was thought that all smooth muscle cells developed in situ exclusively from the splanchnopleuric mesenchyme in the walls of the anlagen of the viscera and around the endothelium of blood vessels. However, recent experimental studies have traced the progeny of cells proliferating from the epithelial plate of the somite and have identified endothelial and tunica media smooth muscle cells arising from individual somites (Scaal & Christ 2004). The origin of the smooth muscle of the iris is still unclear. This region of the eye develops from the optic cup, and so the smooth muscle which arises there is derived either from the neurectoderm of the original optic cup or from the neural crest mesenchyme which later invades the iris.

Following a period of proliferation, clusters of myoblasts become elongated in the same orientation. Dense bodies, associated with actin and cytoskeletal filaments, appear in the cytoplasm, and the surface membrane starts to acquire its specialized features, i.e. caveolae, adherens junctions and gap junctions. Cytoskeletal filaments extend to insert into the submembranous dense plaques and cytoplasmic dense bodies. Thick filaments are seen a few days after the first appearance of thin filaments and intermediate filaments, and from this time the cells are able to contract. During development, dense bodies increase in number and further elements of the cytoskeleton are added. In addition to synthesizing the cytoskeleton and contractile apparatus, the differentiating cells express and secrete components of the extracellular matrix.

In a developing smooth muscle all the cells express characteristics of the same stage of differentiation, and there are no successive waves of differentiation. From its earliest appearance to maturity, a smooth muscle increases several hundredfold in mass, partly by a 2- to 4-fold increase in the size of individual cells, but mainly by a very large increase in cell number. Growth occurs by division of cells in every part of the muscle, not just at its surface or ends. Mitosis occurs in cells in which differentiation is already well advanced, as evidenced by the presence of myofilaments and membrane specializations. Mitotic smooth muscle cells may be found at any stage of life, but their numbers peak before birth, at a time that differs for different muscles; they are rare in the adult unless the tissue is stimulated to hypertrophy (as in the pregnant uterus) or to repair. The ability of mature cells to undergo mitosis therefore differs between the three major types of muscle: skeletal muscle cells cannot divide at all after differentiation; cardiac muscle cells can divide, but only before birth; and smooth muscle cells appear to remain capable of division throughout life.

During the early stages of development, smooth muscle expresses embryonic and non-muscle isoforms of myosin. The proportions of these isoforms decrease progressively. Initially, SM-1 is the dominant or exclusive smooth muscle heavy chain isoform: the SM-2 isoform becomes more established later. For a review of the development of vascular smooth muscle see Owens, Kumar and Wamhoff (2004).



Cells of peripheral blood, suspended in plasma, circulate through the body in the blood vascular system. Interstitial fluid from peripheral tissues returns to the blood vascular system via the lymphatic system, which also provides a channel for the migration of leukocytes and the absorption of certain nutrients from the gut.

The cardiovascular system carries nutrients, oxygen, hormones, etc. throughout the body and the blood redistributes and disperses heat. As a consequence of the hydrostatic pressure, the system also has mechanical effects, such as maintaining tissue turgidity and counteracting the effects of gravity. Blood circulates within a fast, high capacity system made up of the heart, which is the central pump and main motor of the system; arteries, which lead away from the heart and carry the blood to the peripheral parts of the body; and veins, which return the blood to the heart. The heart can be thought of as a pair of muscular pumps, one feeding a minor loop (pulmonary circulation), which serves the lungs and oxygenates the blood, the other feeding a major loop (systemic circulation), which serves the rest of the body. With limited exceptions, each loop is a closed system of tubes, so that blood per se does not usually leave the circulation.

From the centre to the periphery, the vascular tree shows three main modifications. The arteries increase in number by repeated bifurcation and by sending out side branches, in both the systemic and the pulmonary circulation. For example, the aorta, which carries blood from the heart to the systemic circulation, gives rise to about 4 × 106 arterioles and four times as many capillaries. The arteries also decrease in diameter, although not to the same extent as their increase in number, so that a hypothetical cross-section of all the vessels at a given distance will increase in total area with increasing distance from the heart. At its emergence from the heart, the aorta of an adult man has an outer diameter of approximately 30 mm (cross-sectional area of nearly 7 cm2). The diameter decreases along the arterial tree until it is as little as 10 μm in arterioles (each with a cross-sectional area of about 80 μm2). However, given the enormous number of arterioles, the total crosssectional area at this level is approximately 150 cm2, more than 200 times that of the aorta. As a result, blood flow is faster near the heart than at the periphery.

The walls of arteries decrease in thickness towards the periphery, although this is not as substantial as the reduction in vessel diameter. Consequently, in the smallest arteries (arterioles), the thickness of the wall represents about half the outer radius of the vessel, whereas in a large vessel it represents between one-fifteenth and one-fifth, e.g. in the thoracic aorta the radius is approximately 17 mm and the wall thickness 1.1 mm.

Venules, which return blood from the periphery, converge on each other forming a progressively smaller number of veins of increasingly large size. As with arteries, the hypothetical total cross-sectional area of all veins at a given level reduces nearer to the heart. Eventually, only the two largest veins, the superior and inferior venae cavae, open into the heart from the systemic circulation. A similar pattern is found in the pulmonary circulation, but here the vascular loop is shorter and has fewer branch points, and consequently, the number of vessels is smaller than in the systemic circulation. The total end-to-end length of the vascular network in a typical adult is twice the circumference of the earth.

Large arteries, such as the thoracic aorta, subclavian, axillary, femoral and popliteal arteries, lie close to a single vein which drains the same territory as that supplied by the artery. Other arteries are usually flanked by two veins, satellite veins (venae comitantes), which lie on either side of the artery, and have numerous cross-connections: the whole is enclosed in a single connective tissue sheath. The artery and the two satellite veins are often associated with a nerve, and when they are surrounded by a common connective tissue sheath they form a neurovascular bundle.

The close association between the larger arteries and veins in the limbs allows the counterflow exchange of heat to take place. This mechanism promotes heat transfer from arterial to venous blood, and thus helps to preserve body heat. Counterflow heat exchange systems are found in certain organs, e.g. in the testis, where the pampiniform plexus of veins surrounds the testicular artery (this arrangement not only conserves body heat, but also maintains the temperature of the testis below average body temperature). Counterflow ion exchange mechanisms are found in the microcirculation, as in the arterial and venous sinusoids of the vasa recta in the renal medulla. Here, countercurrent exchange retains sodium ions at a high concentration in the medullary interstitium, and efferent venous blood transfers sodium ions to the afferent arterial supply.

Arteries and veins are named primarily according to their anatomical position. In functional terms, three main classes of vessel are described: resistance vessels (arteries, but mainly arterioles), exchange vessels (capillaries, sinusoids and small venules) and capacitance vessels (veins). Structurally, arteries can also be divided into elastic and muscular types. Although muscle cells and elastic tissue are present in all arteries, the relative amount of elastic material is greatest in the largest vessels, whereas the relative amount of smooth muscle increases progressively towards the smallest arteries.

Arteries may also be subdivided into conducting and distributing, as well as resistance, vessels. The large conducting arteries which arise from the heart, together with their main branches, are characterized by the predominantly elastic properties of their walls. Distributing vessels are smaller arteries supplying the individual organs, and their wall is characterized by a well-developed muscular component. Resistance vessels are mainly arterioles. Small and muscular, they provide the main source of the peripheral resistance to blood flow, and they cause a marked drop in the pressure of blood which flows into the capillary beds within tissues.

Capillaries, sinusoids and small (postcapillary) venules are collectively termed exchange vessels. Their walls allow exchange between blood and the interstitial tissue fluid which surrounds all cells: this is the essential function of a circulatory system. Arterioles, capillaries and venules constitute the microvascular bed, the structural basis of the microcirculation.

Larger venules and veins form an extensive, but variable, large-volume, low-pressure system of vessels conveying blood back to the heart. The high capacitance of these vessels is due to the distensibility (compliance) of their walls, so that the content of blood is high even at low pressures. This part of the vascular bed contains the greatest proportion of blood, reflecting the large relative volume of veins.

Blood from the abdominal part of the digestive tube (with the exception of the lower part of the anal canal), and from the spleen, pancreas and gallbladder, drains to the liver via the portal vein. The portal vein ramifies within the substance of the liver like an artery and ends in the hepatic sinusoids. These drain into the hepatic veins which in turn drain into the inferior vena cava. Blood supplying the abdominal organs thus passes through two sets of capillaries before it returns to the heart. The first provides the organs with oxygenated blood, and the second carries deoxygenated blood, rich in absorption products from the intestine, through the liver parenchyma. A venous portal circulation also connects the median eminence and infundibulum of the hypothalamus with the adenohypophysis. In essence, a venous portal system is a capillary network that lies between two veins, instead of between an artery and a vein, which is the more usual arrangement in the circulation. A capillary network may also be interposed between two arteries, e.g. in the renal glomeruli, where the glomerular capillary bed lies between afferent and efferent arterioles. This maintains a relatively high pressure system, which is important for renal filtration.

A parallel circulatory system in the body is provided by the lymphatic vessels and lymph nodes. Lymphatic vessels originate in peripheral tissues as blind-ended endothelial tubes which collect excess fluid from the interstitial spaces between cells and conduct it as lymph. Lymph is returned to the blood vascular system via lymphatic vessels which converge on the large veins in the root of the neck.

The development of blood vessels is described on pages, 206–208.

General features of vessel walls

Blood vessels, irrespective of size, and with the exception of capillaries and venules, have walls consisting of three concentric layers (tunicae) (see Fig. 6.7). The intima (tunica intima), is the innermost layer. Its main component, the endothelium, lines the entire vascular tree, including the heart, and the lymphatic vessels. The media (tunica media) is made of muscle tissue, elastic fibres and collagen. While it is by far the thickest layer in arteries, the media is absent in capillaries and is comparatively thin in veins. The adventitia (tunica adventitia) is the outer coat of the vessel, and consists of connective tissue, nerves and vessel capillaries (vasa vasorum). It links the vessels to the surrounding tissues. Vessels differ in the relative thicknesses and detailed compositions of their layers and, in the smallest vessels, the number of layers represented.

Large elastic arteries

The aorta and its largest branches (brachiocephalic, common carotid, subclavian and common iliac arteries) are large elastic arteries which conduct blood to the medium-sized distributing arteries.

The intima is made of an endothelium, resting on a basal lamina, and a subendothelial connective tissue layer. The endothelial cells are flat, elongated and polygonal in outline, with their long axes parallel to the direction of blood flow (see Fig. 6.17). The subendothelial layer is well developed, contains elastic fibres and type I collagen fibrils, fibroblasts and small, smooth muscle-like myointimal cells. The latter accumulate lipid with age and in an extreme form, this feature contributes to atherosclerotic changes in the intima. Thickening of the intima progresses with age and is more marked in the distal than in the proximal segment of the aorta.

A prominent internal elastic lamina, sometimes split, lies between intima and media. This lamina is smooth, measures about 1 μm in thickness, and, with the elastic lamellae of the media, is stretched under the effect of systolic pressure, recoiling elastically in diastole. Elastic arteries thus have the effect of sustaining blood flow despite the pulsatile cardiac output. They also smooth out the cyclical pressure wave. The media has a markedly layered structure, in which fenestrated layers of elastin (elastic lamellae) alternate with interlamellar smooth muscle cells (Fig. 6.6), collagen and fine elastic fibres. The arrangement is very regular, such that each elastic lamella and adjacent interlamellar zone is regarded as a ‘lamellar unit’ of the media. In the human aorta there are approximately 52 lamellar units, measuring about 11 μm in thickness. Number and thickness of lamellar units increases during postnatal development, from 40 at birth.

The adventitia is well developed. In addition to collagen and elastic fibres, it contains flattened fibroblasts with extremely long, thin processes, macrophages and mast cells, nerve bundles and lymphatic vessels. The vasa vasorum are usually confined to the adventitia.

Muscular arteries

Muscular arteries are characterized by the predominance of smooth muscle in the media (Fig. 6.8). The intima consists of an endothelium, similar to that of elastic arteries, which rests on a basal lamina and subendothelial connective tissue. The internal elastic lamina (Fig. 6.7, Fig. 6.8) is a distinct, thin layer, sometimes duplicated and occasionally absent. It is thrown into wavy folds as a result of contraction of smooth muscle in the media. Some 75% of the mass of the media consists of smooth muscle cells which run spirally or circumferentially around the vessel wall. The relative amount of extracellular matrix is therefore less than in large arteries, however, fine elastic fibres which run mainly parallel to the muscle cells are present. An external elastic lamina, composed of sheets of elastic fibres, forms a less compact layer than the internal lamina, and separates the media from the adventitia in the larger muscular arteries. The adventitia is made of fibroelastic connective tissue, and can be as thick as the media in the smaller arteries. The inner part of the adventitia contains more elastic than collagen fibres.


In arterioles (Fig. 6.9, Fig. 6.10) the endothelial cells are smaller than in large arteries, but their nuclear region is thicker and often projects markedly into the lumen. The nuclei are elongated and orientated parallel to the vessel length, as is the long axis of the cell. The basal surface of the endothelium contacts a basal lamina, but an internal elastic lamina is either absent or is highly fenestrated and traversed by the cytoplasmic processes of muscle cells or endothelial cells.

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