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.
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When the light chains are phosphorylated, they become active and will allow contraction to occur. 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 MLC 20 light chain, which causes a conformational change that increases the angle in the neck domain of the myosin heavy chain,  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.
Phosphorylation of the MLC 20 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, MLC 20 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 slowing the progression to the cycle stage whereby dephosphorylated myosin detaches from the actin, thereby maintaining the force at low energy costs.
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 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 MLC 20 myosin light chains and thereby inhibits contraction. Nitric oxide and PGI2 stimulate soluble guanylate cyclase and membrane bound adenylate cyclase, respectively.
The phosphorylation events lead to a decrease in intracellular 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 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. 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. The contractile function of vascular smooth muscle regulates the lumenal diameter of the small arteries-arterioles called resistance vessels, thereby contributing significantly to setting the level of blood pressure and blood flow to vascular beds.
Smooth muscle contracts slowly and may maintain the contraction tonically for prolonged periods in blood vessels, bronchioles, and some sphincters. 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 proliferation is implicated in the pathogenesis of atherosclerosis and is inhibited by nitric oxide. The embryological origin of smooth muscle is usually of mesodermal origin, after the creation of muscle fibers in a process known as myogenesis.
Sinoatrial (SA) Node
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. 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 malignant neoplasm that can be found in the inferior vena cava , pulmonary arteries and veins , and other peripheral vessels.
Cardiac Muscle Tissue | Boundless Anatomy and Physiology
See Atherosclerosis. From Wikipedia, the free encyclopedia. Archived from the original on 1 February Retrieved 28 April Authors: Stephen M. Schwartz, Robert P. Editors: Stephen M. Contributors: Stephen M. Publisher: Academic Press, Single muscle fibre contractile properties in young and old men and women. J Physiol , Berlin, Springer, ; Chapter 46, Table Muscular system. Fusiform Pennate muscle Unipennate Bipennate.
Anatomical terms of muscle Origin Insertion List of muscles of the human body Composite muscle. Muscle tissue. Calmodulin Vascular smooth muscle. Sarcospan Laminin, alpha 2. NOS1 Caveolin 3. Epimysium Fascicle Perimysium Endomysium Connective tissue in skeletal muscle.
Calcium Cycling in Synthetic and Contractile Phasic or Tonic Vascular Smooth Muscle Cells
Neuromuscular junction Motor unit Muscle spindle Excitation—contraction coupling Sliding filament mechanism. Myocardium Intercalated disc Nebulette. Mammalian skeletal muscle. A A single muscle fiber surrounded by its sarcolemma has been cut away to show individual myofibrils. The cut surface of the myofibrils shows the arrays of thick and thin filaments. The sarcoplasmic reticulum with its transverse T tubules and terminal cisterns surrounds each Forgot Password? What is MyAccess? Otherwise it is hidden from view. Forgot Username?
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