Psychology Wiki

Assessment | Biopsychology | Comparative | Cognitive | Developmental | Language | Individual differences | Personality | Philosophy | Social |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |

Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)

File:Glatte Muskelzellen.jpg

Smooth muscle

File:Illu esophageal layers.jpg

Layers of Esophageal 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

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, 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 are spindle-shaped, and, like striated muscle, can tense and relax. In the relaxed state, each cell is spindle-shaped, 20-500 micrometers in is ~6:1 in striated muscle and ~15:1 in smooth muscle.[How to reference and link to summary or text] 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.


To maintain organ dimensions against forces, 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 dynamic or Cajal pacemaker cells) or be induced by a number of physiochemical agents (e.g., hormones, drugs, neurotransmitters - particularly from the autonomic nervous system), and also mechanical stimulation (such as stretch).

Smooth muscles have been divided into "single unit" and "multi-unit" or into "phasic" and "tonic" types based on the characteristics of the contractile patterns and characteristics of the smooth muscle. Multi-unit smooth muscle lines the large airways to the lungs and large blood vessels. The ciliary muscles within the eye and the arrector pili muscle of the skin are also multiunit. This smooth muscle contains few gap junctions and the autonomic nervous system innervates each smooth cell and regulates them like motor units so graded responses can occur. Single unit smooth muscle lines all the hollow organs and is most common. This type 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, vagina etc. is different in their expression of ionic channels, hormone receptors, cell-signaling pathways, and other proteins that determine function. 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.

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.


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.

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.


  1. 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

Muscular system - edit
Muscular tissue | Muscle contraction | Muscles of the human body
Muscular types
Cardiac muscle | Skeletal muscle | Smooth muscle
This page uses Creative Commons Licensed content from Wikipedia (view authors).