smooth muscle
| Dictionary: smooth muscle |
n.
Muscle tissue that contracts without conscious control, having the form of thin layers or sheets made up of spindle-shaped, unstriated cells with single nuclei and found in the walls of the internal organs, such as the stomach, intestine, bladder, and blood vessels, excluding the heart.
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| World of 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.
| Dental Dictionary: smooth muscle |
n
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.
| Sports Science and Medicine: smooth muscle |
involuntary 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.
Smooth muscle
| Wikipedia: Smooth muscle |
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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
Smooth muscle is an involuntary non-striated muscle, found within the tunica media layer of large and small arteries and veins, the bladder, uterus, male and female reproductive tracts, gastrointestinal tract, respiratory tract, arrector pili of skin, the ciliary muscle, and iris of the eye. The glomeruli of the kidneys contain a smooth muscle-like cell called the mesangial cell. Smooth muscle is fundamentally different from skeletal muscle and cardiac muscle in terms of structure, function, excitation-contraction coupling, and mechanism of contraction.
Smooth muscle fibers have fusiform shape, and, like striated muscle, can tense and relax. In the relaxed state, each cell is spindle-shaped, 20-500 micrometers in length. The ratio of actin to myosin is ~6:1 in striated muscle and ~15:1 in smooth muscle.[citation needed] 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.
However, there is an organized cytoskeleton consisting of the intermediate filament proteins vimentin and desmin, along with actin filaments. Actin filaments attach to the sarcolemma by focal adhesions or in a spiral corkscrew fashion, and contractile proteins can organize into zones of actin and myosin along the axis of the cell.
The sarcolemma possess microdomains specialized to cell-signaling events and ion channels called caveolae. 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 in close proximity to sarcoplasmic reticulum or mitochondria, and have been proposed to organize signaling molecules in the membrane.
Contents |
Function
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. Smooth muscle may contract spontaneously (via ionic channel dynamics or as in the gut special pacemakers cells interstitial cells of Cajal produce rhythmic contractions, or be induced by a number of physiochemical agents (e.g., hormones, drugs, neurotransmitters - particularly from the autonomic nervous system), and innervates each smooth cell and regulates them like motor units so graded responses can occur. Single unit smooth muscle is most common and lines blood vessels, the urinary tract, and the digestive tract. This type of smooth muscle tends to contract rhythmically, is coupled by numerous gap junctions, and often exhibits spontaneous action potential. Another nomenclature separates smooth muscle by contractile pattern. It 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. For example, contractile function of vascular smooth muscle is critical to regulating the lumenal diameter of the small arteries-arterioles called resistance vessels. The resistance arteries contribute 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. 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. 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.
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. Specialized smooth muscle within the afferent arteriole of the juxtaglomerular apparatus secretes renin in response to osmotic and pressure changes. Renin in turn activates the angiotensin system to regulate blood presure. Smooth muscle-containing tissue often must be stretched, 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. These fibers with their extracellular matrices contribute to the viscoelasticity of these tissues. Smooth muscle also has specific elastin and collagen receptors to interact with these proteins.
Contraction and relaxation basics
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 adopt their original conformation. They can then re-bind to another part of 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 cannot occur until the myosin heads have been activated to allow crossbridges to form. The myosin heads are made up of heavy chains and light protein chains. 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). 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. The phosphorylation of the light chains by MLCK is countered by a myosin light-chain phosphatase, which dephosphorylates the myosin light chains and inhibits the contraction. 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.
Phosphorylation of the 20 kd 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, 20 kd myosin light chains phosphorylation decreases, and energy utilization decreases and the muscle can relax, however there is a sustained maintenance of force in vascular smooth muscle. The sustained phase has been attributed to slowly cycling dephosphorylated myosin crossbridges termed latch-bridges and actin polymerization stiffening the cell. During contraction of muscle, rapidly cycling crossbridges form between activated actin and phosphorylated myosin generating force. During the sustained phase, phosphorylation levels decline and slow cycling dephosphorylated crossbridges act as latch bridges to contribute to maintaining the force at low energy costs. Other cell signaling pathways and protein kinases (Protein kinase C, ROCK 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. 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 form interacting with actin.
Advances and Current Research in Contraction and Relaxation
Muscle can be characterized as two types: tonic and phasic which describes their response to depolarizing high potassium solutions. Tonic smooth muscle contracts and relaxes slowly and exhibits force maintenance such as vascular smooth muscle. Force maintenance is the maintaining of a contraction for a prolonged time with little energy utilization. The phasic smooth muscle contracts and relaxes rapidly such as gut smooth muscle. This phasic response is useful to massage substances through the lumen of the gastrointestinal tract during peristalsis. Vascular smooth muscle (walls of arteries and veins) and visceral smooth muscle (wall of gastrointestinal tract, urogenital tract, iris) is another distinction in common use to discriminate the kind of smooth muscle. Contractions in vertebrate smooth muscle can be initiated by stretch, gap junction electrical, and neural and humoral receptor mediated agents (acetylcholine, endothelin, etc.). Smooth muscle in the gastrointestinal and urogenital tracts is regulated by the enteric nervous system and by peristaltic pacemaker cells -- the interstitial cells of Cajal.
Stretch, neural and humoral agents, and gap junction activity that depolarize the sarcolemma increase intracellular calcium. Extracellular calcium enters through L type calcium channels and intracellular calcium is released from stored calcium in the sarcoplasmic reticulum. Calcium release from the sarcoplasmic reticulum is through Ryanodine receptor channels (calcium sparks) by a redox process and inositol triphosphate receptor channels by the second messenger inositol triphosphate. The intracellular calcium binds with calmodulin which then binds and activates myosin-light chain kinase. The calcium-calmodulin-myosin light chain kinase complex phosphorylates the 20 kilodalton (kd) myosin light chains on amino acid residue-serine 19 to initiate contraction. The phosphorylation of the myosin light chains then allows the myosin ATPase to function. The thin filament associated proteins caldesmon and calponin are also believed to serve a function in contractility within smooth muscle. During contraction actin polymerization also occurs and it appears to be significant in the process.
Phosphorylation of the 20 kd 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, 20 kd myosin light chains phosphorylation decreases, and energy utilization decreases and the muscle can relax, however there is a sustained maintenance of force in vascular smooth muscle. The sustained phase has been attributed to slowly cycling dephosphorylated myosin crossbridges termed latch-bridges and actin polymerization stiffening the cell. During contraction of muscle, rapidly cycling crossbridges form between activated actin and phosphorylated myosin generating force. During the sustained phase, phosphorylation levels decline and slow cycling dephosphorylated crossbridges act as latch bridges to contribute to maintaining the force at low energy costs. Other cell signalling pathways and protein kinases (Protein kinase C, ROCK kinase, Zip kinase, Focal adhesion kinases) have been implcated and actin polymerization dynamics plays a role in force maintenance. While myosin light chain phosphorylation correlates well with shortening velocity, other cell signalling 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.
Phosphorylation of the 20kd myosin light chains is counteracted by a myosin light chain phosphatase that dephosphorylates the myosin light chains. 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.
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. These cyclic nucleotides 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 envolved in this process. 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.
Recent research indicates that sphingosine-1-phosphatekkoo (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.[1]
Invertebrate smooth muscle
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 molusks use this catch phase of smooth muscle to keep their shell closed for prolonged periods with little energy usage.
Control
Smooth muscle cells can be stimulated to contract or relax in many different ways. They may be directly stimulated by the autonomic nervous system ("involuntarily" control), but can also react on stimuli from neighbouring cells and on hormones (vasodilators or vasoconstrictor) within the medium that it carries. Specialized smooth muscle cells within the afferent arteriole of the juxtaglomerular apparatus of kidney produces renin which activates the angiotension II system.
Growth and rearrangement
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.
Related diseases
"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.
See Asthma.
References
- ^ Scherer EQ et al. Sphingosine-1-phosphate modulates spiral modiolar artery tone: A potential role in vascular-based inner ear pathologies? Cardiovasc Res. 2006 Apr 1;70(1):79-87.
See also
External links
- BBC - baby born with smooth muscle condition has 8 organs transplanted
- Smooth muscle antibody
- Stomach smooth muscle identified using antibody
- UIUC Histology Subject 265
- Histology at KUMC muscular-muscle08 "Smooth Muscle"
- Histology at BU 21701ooa
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