Talk:Smooth muscle

message: Someone please correct the sentence "each cell is spindle-shaped, 20-500 micrometers in is ~6:1 in striated muscle and ~15:1 in smooth muscle" - perhaps it's about cell length:width proportions, but I always thought that smooth muscles are less elongated than striated.Porridge (talk) 09:49, 23 May 2009 (UTC)
replies: text: I made the Function section a bit easier to read. Jamesters 23:22, 16 November 2006 (UTC)

text: All right, that makes sense. Thanks for clarifying! Jamesters 10:58, 17 November 2006 (UTC)
replies: text: What206.74.157.2 (talk) 15:10, 15 April 2011 (UTC)
thread_title: Untitled

message: :::The advanced section of contraction and relaxation is great info but probably not appropriate for this encyclopedia. I paired the article down by removing section so we can fix this article. I believe some of the info can be mentioned in other articles or perhaps another article with a different emphasis or cherry pick some to put in basic section. I will move the section to here for now:
Section on Advanced Contraction and Relaxation removed for development.
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.GetAgrippa (talk) 15:38, 21 November 2007 (UTC)
replies: text: There is now a discussion of latch bridges. To my knowledge their aren't any volutary smooth muscles. All the smooth muscle sphincters are involuntary and skeletal muscle sphincters are voluntarily regulated. Smooth muscle in eyes, kidneys, arteries and veins, gut, bladder and reproductive tract, are involuntary. Smooth muscle in skin is also involuntary.GetAgrippa (talk) 01:34, 20 June 2009 (UTC)
thread_title: Advanced section

message: I'm going to use the talk page as a sandbox while I gather references for this article. I will later format by Wikipedia standards. GetAgrippa (talk) 15:57, 14 December 2009 (UTC)
thread_title:  Time to add references

message: Thanks to all the editors who took my effort to expand this article and organized and expanded it. I still think some of my suggestions I posited above would be nice additions still. I added some references here but never incorporated so I'll try to do that. Regards. GetAgrippa (talk) 18:36, 24 January 2014 (UTC)
thread_title: Thanks

message: This sentence in the section 'External substances' is contradictory as regards adrenergic receptors in the smooth muscle. Blood vessel contraction is always caused by the smooth muscle of their walls, but the sentence starts saying they have alpha-1-adrenergic receptors but ends saying they have beta-adrenergic receptors. The sentence is: "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." What does 'most blood vessels' mean here? Most blood vessels in the entire body? Or in the smooth muscle?-Miguelferig (talk) 12:04, 2 November 2014 (UTC)
thread_title:  Adrenergic receptors (confounding sentence) 

message: Small stub covered mostly on target page - the other type is multiunit  another smaller stub without a target which would fit well into  both items being covered on target page structure section Iztwoz (talk) 20:13, 7 April 2022 (UTC)
thread_title:  Proposed merge of [[Single-unit smooth muscle]] into [[Smooth muscle]] 

message: I want to now plesase tell me 103.95.164.129 (talk) 13:21, 21 May 2024 (UTC)
thread_title:  Who discovered smooth muscle cell