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American Heritage Dictionary:
smooth muscle |
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Oxford Companion to the Body:
smooth muscle |
The cardiovascular, gastrointestinal, genitourinary, and respiratory systems are composed mostly of hollow organs (tubular or sacular), which transport and/or store fluids (either liquids or gases) within the body. The walls of these organs contain smooth muscle, a type of tissue which enables them to constrict or dilate, in this way retarding or facilitating fluid movement as required. This is accomplished by the shortening or lengthening of the individual smooth muscle cells, which occurs in a co-ordinated fashion because the cells are electrically coupled by intercellular connections, known as gap junctions. Other structures in the body that contain smooth muscle include the myometrium — the muscular wall of the uterus — which is responsible for the rhythmic contractions of labour; the piloerector muscles, which cause skin hair to stand up; and the irises, which control the diameter of the pupils.
Smooth muscle thus subserves all internal, involuntary functions, except the movements of breathing and the beating of the heart. Many directly acting chemical agents affect its contraction, but most smooth muscle is also under the control of the autonomic nervous system; in some sites (notably most blood vessels) it is influenced only by the sympathetic component, and at others (for example in the gut and the iris) by dual, and sometimes opposite, effects of sympathetic and parasympathetic nerves.
As befits its many functions, smooth muscle at different sites is much more heterogeneous than skeletal or cardiac muscle. By creating diverse structural arrangements of smooth muscle and other associated cells, and at the same time varying the mechanisms that control contraction, evolution has achieved a remarkable diversity of smooth muscle-containing organs, each of which is designed to fill a unique functional niche.
Calcium and contraction
On a cellular level, however, all smooth muscles share many characteristics. When relaxed, the cells assume the shape of long, narrow spindles or worms. The cells are termed ‘smooth’ because they lack the regular bands or striations which are prominent in skeletal muscle fibres and cardiac muscle cells. Smooth muscle cells are capable of contracting dramatically, to half or less of their relaxed length. Contraction may be sustained, as in the smooth muscle cells present in the blood vessels or airways, or rhythmic, as in the cells of the myometrium and gastrointestinal tract. The main stimulus for contraction is a rise in the cellular concentration of calcium. This can be triggered by an impressive array of chemical signals, that differ depending on the type of smooth muscle involved, including a variety of neurotransmitters released at autonomic nerve endings.
As in striated muscles, contraction occurs because the rise in cellular calcium causes an interaction between cellular action and myosin filaments, although the arrangement of these filaments within the cells is not of a similar consistent pattern. Also, the mechanism whereby calcium stimulates this interaction in smooth muscle differs from that in striated muscle, in that it involves activation of a different signalling protein (calmodulin rather than troponin). Another important difference between smooth and striated muscle is that smooth muscle never becomes fatigued, because it uses metabolic energy much more efficiently than does striated muscle.
In common experience, some obvious manifestations of altered smooth muscle activity are the widening of the pupils in the dark when the radially arranged muscle of the iris contracts; asthmatic wheezing, when the smooth muscle in the walls of the bronchioles impedes airflow; and the phenomenon of erection, when blood vessel relaxation allows engorgement.
Self-regulating pipes
The functioning of each type of smooth muscle is intimately tied up with the organ or system of which it is a part, so that this type of tissue is perhaps best appreciated if one abandons the attempt to generalize and considers, for example, the blood vessels.
The arteries and veins are not merely conduits designed to convey blood passively to and from the capillaries. Rather, they exist in a dynamic state of partial constriction, regulated by the smooth muscle cells which form much of the vascular wall, where they are arranged in multiple layers embedded in a tough and elastic matrix of connective tissue. The cells wrap around the vessel in a low-pitch spiral, so that, when they shorten, the vascular lumen is constricted. The layers of smooth muscle cells are separated from the blood by a monolayer of flat, polygonal endothelial cells. These remarkable cells carry out multiple vital tasks, which include controlling the clotting of blood and releasing substances which influence the contraction and also the growth of the smooth muscle cells. The most important of these substances, nitric oxide, is a short-lived gas which reacts with the protein guanylyl cyclase in the smooth muscle cells, causing them to relax and lengthen. Nitric oxide release is controlled by many factors, including the friction exerted by the flowing blood, and also by hormones and other messenger molecules present in the blood.
The outer layer of blood vessels contains nerves of the sympathetic component of the autonomic nervous system, the activity of which is controlled by the brain. The sympathetic nerve endings are constantly releasing minute quantities of norepinephrine (also called ‘noradrenaline’), a neurotransmitter which stimulates the smooth muscle cells to shorten. The length of the smooth muscle cells, and therefore the diameter of the blood vessel, is largely determined by the ongoing balance between the opposing influences on constriction of nitric oxide and norepinephrine.
These factors account for the dynamic state of partial constriction of the blood vessels, of which the overall effect is to impose a net resistance to the flow of blood from the heart; along with cardiac output, this is an important determinant of blood pressure. This resistance can be varied by alterations in the levels of norepinephrine release and nitric oxide production; by a myriad of other factors such as local tissue acidity, the oxygen concentration in the blood, temperature; and also by other hormones which can stimulate or inhibit smooth muscle cell shortening.
Apart from variation in the overall net resistance to blood flow, the degree of constriction or relaxation varies from region to region in different physiological circumstances. For example, although during strenuous exercise the heart may increase its pumping rate by about five times, the rate of delivery blood to each organ does not increase by this amount. Instead, the combined effects of activation of the sympathetic nervous system, and the release of substances generated in the heart and working muscles, causes the arteries in the heart and muscles to dilate dramatically, while the arteries in the non-working muscle and the digestive organs constrict. In this way, the flow of blood and therefore of oxygen to the muscles and to the heart may increase by twenty- and five-fold respectively, while the flow of blood to the rest of the body, excepting the brain, actually falls. Conversely, at rest after a meal, it is the vessels of the digestive organs which dilate.
The humble workhorse
In the gut, the smooth muscle is responsible for the many types of motility — peristalsis, which moves the contents along; relaxation, which accommodates a meal in the stomach; various churning and mixing movements; and finally expulsion of faeces — assisted by voluntary action.
Analogous changes in the functioning of the smooth muscles embedded in other organs are needed to support an enormous variety of involuntary activities, ranging from childbirth and ejaculation to urination, digestion, and visual adjustment to darkness and light. Indeed, as it faithfully performs its various automatically controlled tasks, this humble cousin of the heart and voluntary muscles plays many vital but unheralded roles in shaping both the most dramatic and the most routine events of our lives.
— Philip Aaronson
See also alimentary system; autonomic nervous system; blood vessels; lungs.
Oxford Dictionary of Sports Science & Medicine:
smooth muscle |
Muscle consisting of spindle-shaped cells with no obvious striations. Smooth muscle lines the walls of hollow organs such as the stomach, intestines, and blood vessels. It is particularly well adapted to producing long, slow contractions that are not under voluntary control. Compare striated muscle.
Oxford Dictionary of Biochemistry:
smooth muscle |
| smooth endoplasmic reticulum, smooth, smectic | |
| smooth-rough variation, sn-, snRNA |
Mosby's Dental Dictionary:
smooth muscle |
The simplest of the three types of muscle (smooth, striated, and cardiac). It is the muscle of the lining of the digestive tract, ducts of glands, and viscera associated with the gut. It also supplies the muscles for the genitourinary tract, structures of the blood vessels, connective tissues of the mucous membranes, and skin with its appendages. A typical smooth muscle fiber is a slender, spindle-shaped body averaging a few tenths of a millimeter in length. There is a single, centrally striated nucleus. The cytoplasm appears homogeneous. The cells are arranged in bands, or bundles, with interspersed connective tissue fibers uniting them into an effective common mass. Smooth muscle fibers are innervated in part by nerve fibers and in part by the contraction of adjacent muscle tissues. The digestive tract, particularly, demonstrates waves of contraction that pass along a band of smooth muscle.
Wikipedia on Answers.com:
Smooth muscle tissue |
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This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (August 2008) |
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| Layers of loalol muscle wich is a type of s,mo Wall: 1. Mucosa 2. Submucosa 3. Muscularis 4. Adventitia 5. Striated muscle 6. Striated and smooth 7. Smooth muscle 8. Lamina muscularis mucosae 9. Esophageal glands |
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| Latin | textus muscularis levis; textus muscularis nonstriatus |
| Code | TH H2.00.05.1.00001 |
Smooth muscle is an involuntary non-striated muscle. It is divided into two sub-groups; the single-unit (unitary) and multiunit smooth muscle. Within single-unit smooth muscle tissues, the autonomic nervous system innervates a single cell within a sheet or bundle and the action potential is propagated by gap junctions to neighboring cells such that the whole bundle or sheet contracts as a syncytium (i.e., a multinucleate mass of cytoplasm that is not separated into cells). Multiunit smooth muscle tissues innervate individual cells; as such, they allow for fine control and gradual responses, much like motor unit recruitment in skeletal muscle.
Smooth muscle is found within the walls of blood vessels (such smooth muscle specifically being termed vascular smooth muscle) such as in the tunica media layer of large (aorta) and small arteries, arterioles and veins. Smooth muscle is also found in lymphatic vessels, the urinary bladder, uterus (termed uterine smooth muscle), male and female reproductive tracts, gastrointestinal tract, respiratory tract, arrector pili of skin, the ciliary muscle, and iris of the eye. The structure and function is basically the same in smooth muscle cells in different organs, but the inducing stimuli differ substantially, in order to perform individual effects in the body at individual times. In addition, the glomeruli of the kidneys contain smooth muscle-like cells called mesangial cells.
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Most smooth muscle is of the single-unit variety, that is, either the whole muscle contracts or the whole muscle relaxes, but there is multiunit smooth muscle in the trachea, the large elastic arteries, and the iris of the eye. Single unit smooth muscle, however, is most common and lines blood vessels (except large elastic arteries), the urinary tract, and the digestive tract.
Smooth muscle is fundamentally different from skeletal muscle and cardiac muscle in terms of structure, function, regulation of contraction, and excitation-contraction coupling.
Smooth muscle fibers have a fusiform shape and, like striated muscle, can tense and relax. However, smooth muscle containing tissue tend to demonstrate greater elasticity and function within a larger length-tension curve than striated muscle. This ability to stretch and still maintain contractility is important in organs like the intestines and urinary bladder. In the relaxed state, each cell is spindle-shaped, 20-500 micrometers in length.
A substantial portion of the volume of the cytoplasm of smooth muscle cells are taken up by the molecules myosin and actin,[1] which together have the capability to contract, and, through a chain of tensile structures, make the entire smooth muscle tissue contract with them.
Myosin is primarily of class II in smooth muscle.[2]
Different combinations of heavy and light chains allow for up to hundreds of different types of myosin structures, but it is unlikely that more than a few such combinations are actually used or permitted within a specific smooth muscle bed.[2] In the uterus, a shift in myosin expression has been hypothesized to avail for changes in the directions of uterine contractions that are seen during the menstrual cycle.[2]
The thin filaments that form part of the contractile machinery are predominantly composed of α- and γ-actin.[2] Smooth muscle α-actin (alpha actin) is the predominate isoform within smooth muscle. There are also lots of actin (mainly β-actin) that does not take part in contraction, but that polymerizes just below the plasma membrane in the presence of a contractile stimulant and may thereby assist in mechanical tension.[2] Alpha actin is also expressed as distinct genetic isoforms such there is smooth muscle, cardiac muscle and skeletal muscle specific isoforms of alpha actin. (ref The actin gene family: function follows isoform.Perrin BJ, Ervasti JM.Cytoskeleton (Hoboken). 2010 Oct;67(10):630-4. Review.)
The ratio of actin to myosin is between 2:1[2] and 10:1[2] in smooth muscle, compared to ~6:1 in skeletal muscle and 4:1 in cardiac muscle.
Smooth muscle does not contain the protein troponin; instead calmodulin (which takes on the regulatory role in smooth muscle), caldesmon and calponin are significant proteins expressed within smooth muscle.
Also, all three of these proteins may have a role in inhibiting the ATPase activity of the myosin complex that otherwise provides energy to fuel muscle contraction.[2]
The myosin and actin are the contractile parts of continuous chains of tensile structures that stretch both across and between smooth muscle cells.
The actin filaments of contractile units are attached to dense bodies. Dense bodies are rich in α-actinin,[2] and also attach intermediate filaments (consisting largely of vimentin and desmin), and thereby appear to serve as anchors from which the thin filaments can exert force.[2] Dense bodies also are associated with β-actin, which is the type found in the cytoskeleton, suggesting that dense bodies may coordinate tensions from both the contractile machinery and the cytoskeleton.[2]
The intermediate filaments are connected to other intermediate filaments via dense bodies, which eventually are attached to adherens junctions (also called focal adhesions) in the cell membrane of the smooth muscle cell, called the sarcolemma. The adherens junctions consist of large number of proteins including α-actinin, vinculin and cytoskeletal actin.[2] The adherens junctions are scattered around dense bands that are circumfering the smooth muscle cell in a rib-like pattern.[1] The dense band (or dense plaques) areas alternate with regions of membrane containing numerous caveolae. When complexes of actin and myosin contract, force is transduced to the sarcolemma through intermediate filaments attaching to such dense bands.
During contraction, there is a spatial reorganization of the contractile machinery to optimize force development.[2] part of this reorganization consists of vimentin being phosphorylated at Ser56 by a p21 activated kinase, resulting in some disassembly of vimentin polymers.[2]
Also, the number of myosin filaments is dynamic between the relaxed and contracted state in some tissues as the ratio of actin to myosin changes, and the length and number of myosin filaments change.
Smooth muscle cells have been observed contracting in a spiral corkscrew fashion, and contractile proteins have been observed organizing into zones of actin and myosin along the axis of the cell.
Smooth muscle-containing tissue needs to be stretched often, so elasticity is an important attribute of smooth muscle. Smooth muscle cells may secrete a complex extracellular matrix containing collagen (predominantly types I and III), elastin, glycoproteins, and proteoglycans. Smooth muscle also has specific elastin and collagen receptors to interact with these proteins of the extracellular matrix. These fibers with their extracellular matrices contribute to the viscoelasticity of these tissues. For example, the great arteries are viscolelastic vessels that act like a Windkessel, propagating ventricular contraction and smoothing out the pulsatile flow, and the smooth muscle within the tunica media contributes to this property.
The sarcolemma also contains caveolae, which are microdomains of lipid rafts specialized to cell-signaling events and ion channels. These invaginations in the sarcoplasma contain a host of receptors (prostacyclin, endothelin, serotonin, muscarinic receptors, adrenergic receptors), second messenger generators (adenylate cyclase, Phospholipase C), G proteins (RhoA, G alpha), kinases (rho kinase-ROCK, Protein kinase C, Protein Kinase A), ion channels (L type Calcium channels, ATP sensitive Potassium channels, Calcium sensitive Potassium channels) in close proximity. The caveolae are often close to sarcoplasmic reticulum or mitochondria, and have been proposed to organize signaling molecules in the membrane.
A smooth muscle is excited by external stimuli, which causes contraction. Each step is further detailed below.
Smooth muscle may contract spontaneously (via ionic channel dynamics) or as in the gut special pacemakers cells interstitial cells of Cajal produce rhythmic contractions. Also, contraction, as well as relaxation, can be induced by a number of physiochemical agents (e.g., hormones, drugs, neurotransmitters - particularly from the autonomic nervous system.
Smooth muscle in various regions of the vascular tree, the airway and lungs, kidneys and vagina is different in their expression of ionic channels, hormone receptors, cell-signaling pathways, and other proteins that determine function.
For instance, most blood vessels respond to norepinephrine and epinephrine (from sympathetic stimulation or the adrenal medulla) by producing vasoconstriction (this response is mediated through alpha 1-adrenergic receptors). Blood vessels in skeletal muscle and cardiac muscle respond to these catecholamines producing vasodilation because the smooth muscle possess beta-adrenergic receptors.
Generally, arterial smooth muscle responds to carbon dioxide by producing vasodilation, and responds to oxygen by producing vasoconstriction. Pulmonary blood vessels within the lung are unique as they vasodilate to high oxygen tension and vasoconstrict when it falls. Bronchiole, smooth muscle that line the airways of the lung, respond to high carbon dioxide producing vasodilation and vasoconstrict when carbon dioxide is low. These responses to carbon dioxide and oxygen by pulmonary blood vessels and bronchiole airway smooth muscle aid in matching perfusion and ventilation within the lungs. Further different smooth muscle tissues display extremes of abundant to little sarcoplasmic reticulum so excitation-contraction coupling varies with its dependence on intracellular or extracellular calcium.
Recent research indicates that sphingosine-1-phosphate (S1P) signaling is an important regulator of vascular smooth muscle contraction. When transmural pressure increases, sphingosine kinase 1 phosphorylates sphingosine to S1P, which binds to the S1P2 receptor in plasma membrane of cells. This leads to a transient increase in intracellular calcium, and activates Rac and Rhoa signaling pathways. Collectively, these serve to increase MLCK activity and decrease MLCP activity, promoting muscle contraction. This allows arterioles to increase resistance in response to increased blood pressure and thus maintain constant blood flow. The Rhoa and Rac portion of the signaling pathway provides a calcium-independent way to regulate resistance artery tone.[4]
To maintain organ dimensions against force, cells are fastened to one another by adherens junctions. As a consequence, cells are mechanically coupled to one another such that contraction of one cell invokes some degree of contraction in an adjoining cell. Gap junctions couple adjacent cells chemically and electrically, facilitating the spread of chemicals (e.g., calcium) or action potentials between smooth muscle cells. Single unit smooth muscle displays numerous gap junctions and these tissues often organize into sheets or bundles which contract in bulk.
Smooth muscle contraction is caused by the sliding of myosin and actin filaments (a sliding filament mechanism) over each other. The energy for this to happen is provided by the hydrolysis of ATP. Myosin functions as an ATPase utilizing ATP to produce a molecular conformational change of part of the myosin and produces movement. Movement of the filaments over each other happens when the globular heads protruding from myosin filaments attach and interact with actin filaments to form crossbridges. The myosin heads tilt and drag along the actin filament a small distance (10-12 nm). The heads then release the actin filament and then changes angle to relocate to another site on the actin filament a further distance (10-12 nm) away. They can then re-bind to the actin molecule and drag it along further. This process is called crossbridge cycling and is the same for all muscles (see muscle contraction). Unlike cardiac and skeletal muscle, smooth muscle does not contain the calcium-binding protein troponin. Contraction is initiated by a calcium-regulated phosphorylation of myosin, rather than a calcium-activated troponin system.
Crossbridge cycling causes contraction of myosin and actin complexes, in turn causing increased tension along the entire chains of tensile structures, ultimately resulting in contraction of the entire smooth muscle tissue.
Smooth muscle may contract phasically with rapid contraction and relaxation, or tonically with slow and sustained contraction. The reproductive, digestive, respiratory, and urinary tracts, skin, eye, and vasculature all contain this tonic muscle type. This type of smooth muscle can maintain force for prolonged time with only little energy utilization. There are differences in the myosin heavy and light chains that also correlate with these differences in contractile patterns and kinetics of contraction between tonic and phasic smooth muscle.
Crossbridge cycling cannot occur until the myosin heads have been activated to allow crossbridges to form. When the light chains are phosphorylated, they become active and will allow contraction to occur. The enzyme that phosphorylates the light chains is called myosin light-chain kinase (MLCK), also called MLC20 kinase.[2] In order to control contraction, MLCK will work only when the muscle is stimulated to contract. Stimulation will increase the intracellular concentration of calcium ions. These bind to a molecule called calmodulin, and form a calcium-calmodulin complex. It is this complex that will bind to MLCK to activate it, allowing the chain of reactions for contraction to occur.
Activation consists of phosphorylation of a serine on position 19 (Ser19) on the MLC20 light chain, which causes a conformational change that increases the angle in the neck domain of the myosin heavy chain,[2] which corresponds to the part of the cross-bridge cycle where the myosin head is unattached to the actin filament and relocates to another site on it. After attachment of the myosin head to the actin filament, this serine phosphorylation also activates the ATPase activity of the myosin head region to provide the energy to fuel the subsequent contraction.[2] Phosphorylation of a threonine on position 18 (Thr18) on MLC20 is also possible and may further increase the ATPase activity of the myosin complex.[2]
Phosphorylation of the MLC20 myosin light chains correlates well with the shortening velocity of smooth muscle. During this period there is a rapid burst of energy utilization as measured by oxygen consumption. Within a few minutes of initiation the calcium level markedly decrease, MLC20 myosin light chains phosphorylation decreases, and energy utilization decreases and the muscle can relax. Still, smooth muscle has the ability of sustained maintenance of force in this situation as well. This sustained phase has been attributed to certain myosin crossbridges, termed latch-bridges, that are cycling very slowly, notably at the cycle stage where dephosphorylated myosin complexes detach from the actin, thereby maintaining the force at low energy costs.[2] This phenomenon is of great value especially for tonically active smooth muscle.[2]
Isolated preparations of vascular and visceral smooth muscle contract with depolarizing high potassium balanced saline generating a certain amount of contractile force. The same preparation stimulated in normal balanced saline with an agonist such as endothelin or serotonin will generate more contractile force. This increase in force is termed calcium sensitization. The myosin light chain phosphatase is inhibited to increase the gain or sensitivity of myosin light chain kinase to calcium. There are number of cell signalling pathways believed to regulate this decrease in myosin light chain phosphatase: a RhoA-Rock kinase pathway, a Protein kinase C-Protein kinase C potentiation inhibitor protein 17 (CPI-17) pathway, telokin, and a Zip kinase pathway. Further Rock kinase and Zip kinase have been implicated to directly phosphorylate the 20kd myosin light chains.
Other cell signaling pathways and protein kinases (Protein kinase C, Rho kinase, Zip kinase, Focal adhesion kinases) have been implicated as well and actin polymerization dynamics plays a role in force maintenance. While myosin light chain phosphorylation correlates well with shortening velocity, other cell signaling pathways have been implicated in the development of force and maintenance of force. Notably the phosphorylation of specific tyrosine residues on the focal adhesion adapter protein-paxillin by specific tyrosine kinases has been demonstrated to be essential to force development and maintenance. For example, cyclic nucleotides can relax arterial smooth muscle without reductions in crossbridge phosphorylation, a process termed force suppression. This process is mediated by the phosphorylation of the small heat shock protein, hsp20, and may prevent phosphorylated myosin heads from interacting with actin.
The phosphorylation of the light chains by MLCK is countered by a myosin light-chain phosphatase, which dephosphorylates the MLC20 myosin light chains and thereby inhibits contraction.[2] Other signaling pathways have also been implicated in the regulation actin and myosin dynamics. In general, the relaxation of smooth muscle is by cell-signaling pathways that increase the myosin phosphatase activity, decrease the intracellular calcium levels, hyperpolarize the smooth muscle, and/or regulate actin and myosin dynamics.
The relaxation of smooth muscle can be mediated by the endothelium-derived relaxing factor-nitric oxide, endothelial derived hyperpolarizing factor (either an endogenous cannabinoid, cytochrome P450 metabolite, or hydrogen peroxide), or prostacyclin (PGI2). Nitric oxide and PGI2 stimulate soluble guanylate cyclase and membrane bound adenylate cyclase, respectively. The cyclic nucleotides (cGMP and cAMP) produced by these cyclases activate Protein Kinase G and Proten Kinase A and phosphorylate a number of proteins. The phosphorylation events lead to a decrease in intracelluar calcium (inhibit L type Calcium channels, inhibits IP3 receptor channels, stimulates sarcoplasmic reticulum Calcium pump ATPase), a decrease in the 20kd myosin light chain phosphorylation by altering calcium sensitization and increasing myosin light chain phosphatase activity, a stimulation of calcium sensitive potassium channels which hyperpolarize the cell, and the phosphorylation of amino acid residue serine 16 on the small heat shock protein (hsp20)by Protein Kinases A and G. The phosphorylation of hsp20 appears to alter actin and focal adhesion dynamics and actin-myosin interaction, and recent evidence indicates that hsp20 binding to 14-3-3 protein is involved in this process. An alternative hypothesis is that phosphorylated Hsp20 may also alter the affinity of phosphorylated myosin with actin and inhibit contractility by interfering with crossbridge formation. The endothelium derived hyperpolarizing factor stimulates calcium sensitive potassium channels and/or ATP sensitive potassium channels and stimulate potassium efflux which hyperpolarizes the cell and produces relaxation.
In invertebrate smooth muscle, contraction is initiated with the binding of calcium directly to myosin and then rapidly cycling cross-bridges, generating force. Similar to the mechanism of vertebrate smooth muscle, there is a low calcium and low energy utilization catch phase. This sustained phase or catch phase has been attributed to a catch protein that has similarities to myosin light-chain kinase and the elastic protein-titin called twitchin. Clams and other bivalve mollusks use this catch phase of smooth muscle to keep their shell closed for prolonged periods with little energy usage.
Although the structure and function is basically the same in smooth muscle cells in different organs, their specific effects or end-functions differ.
Smooth muscle forms precapillary sphincters in blood vessels in metarterioles which regulates the blood flow in capillary beds of various organs and tissues. The contractile function of vascular smooth muscle also regulates the lumenal diameter of the small arteries-arterioles called resistance vessels, thereby contributing significantly to setting the level of blood pressure. Smooth muscle contracts slowly and may maintain the contraction (tonically) for prolonged periods in blood vessels, bronchioles, and some sphincters. Activating arteriole smooth muscle can decrease the lumenal diameter 1/3 of resting so it drastically alters blood flow and resistance. Activation of aortic smooth muscle doesn't significantly alter the lumenal diameter but serves to increase the viscoelasticity of the vascular wall.
In the digestive tract, smooth muscle contracts in a rhythmic peristaltic fashion, rhythmically forcing foodstuffs through the digestive tract as the result of phasic contraction.
A non-contractile function is seen in specialized smooth muscle within the afferent arteriole of the juxtaglomerular apparatus, which secretes renin in response to osmotic and pressure changes, and also it is believed to secrete ATP in tubuloglomerular regulation of glomerular filtration rate. Renin in turn activates the renin-angiotensin system to regulate blood pressure.
The mechanism in which external factors stimulate growth and rearrangement is not yet fully understood. A number of growth factors and neurohumoral agents influence smooth muscle growth and differentiation. The Notch receptor and cell-signaling pathway have been demonstrated to be essential to vasculogenesis and the formation of arteries and veins.
The embryological origin of smooth muscle is usually of mesodermal origin. However, the smooth muscle within the Aorta and Pulmonary arteries (the Great Arteries of the heart) is derived from ectomesenchyme of neural crest origin, although coronary artery smooth muscle is of mesodermal origin.
"Smooth muscle condition" is a condition in which the body of a developing embryo does not create enough smooth muscle for the gastrointestinal system. This condition is fatal.
Anti-smooth muscle antibodies (ASMA) can be a symptom of an auto-immune disorder, such as hepatitis, cirrhosis, or lupus.
Vascular smooth muscle tumors are very rare. They can be malignant or benign, and morbidity can be significant with either type. Intravascular leiomyomatosis is a benign neoplasm that extends through the veins; angioleiomyoma is a benign neoplasm of the extremities; vascular leiomyosarcomas is a malign neoplasm that can be found in the inferior vena cava, pulmonary arteries and veins, and other peripheral vessels. See Atherosclerosis.
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 | myometrium |
| unstriated |
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 | American Heritage Dictionary. The American Heritage® Dictionary of the English Language, Fourth Edition Copyright © 2007, 2000 by Houghton Mifflin Company. Updated in 2009. Published by Houghton Mifflin Company. All rights reserved. Read more |
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| Oxford Companion to the Body. The Oxford Companion to the Body. Copyright © 2001, 2003 by Oxford University Press. All rights reserved. Read more |
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| Oxford Dictionary of Sports Science & Medicine. The Oxford Dictionary of Sports Science & Medicine. Copyright © Michael Kent 1998, 2006, 2007. All rights reserved. Read more |
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Oxford Dictionary of Biochemistry. Oxford University Press. Oxford Dictionary of Biochemistry and Molecular Biology © 1997, 2000, 2006 All rights reserved. Read more | |
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| Mosby's Dental Dictionary. Mosby's Dental Dictionary. Copyright © 2004 by Elsevier, Inc. All rights reserved. Read more |
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