Talk:Smooth muscle

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Well I messed around and have changed most of the article. It maybe too complicated, and surely needs editing. I can provide references for any facts, but I think some of it is too detailed for an encyclopedia. Help me clip down. GetAgrippa 21:50, 6 October 2006 (UTC)

yeh somebody make the part about function a little less complicated please

I made the Function section a bit easier to read. Jamesters 23:22, 16 November 2006 (UTC)

In my studies,"Smooth muscle tissue" always seemed to be a slang term. The more professional term that was used was "Visceral muscle tissue". Isn't Visceral muscle tissue the official term for it now? Shouldn't this article be renamed? I may be incorrect. I'm not going to change it right now myself since I am not confident enough. It may need to be considered though. Jamesters 23:22, 16 November 2006 (UTC)

Jamesters there is Vascular and Visceral Smooth muscle and it refers to its location. Vascular- arteries and veins or viscera-gut,reproductive tract, respiratory tract, etc.GetAgrippa 01:01, 17 November 2006 (UTC)

All right, that makes sense. Thanks for clarifying! Jamesters 10:58, 17 November 2006 (UTC)

Is someone able to explain "slow waves rhythm" (don't know exact English term), decribed in Guyton's physiology as a process characterictic to smooth muscles, that can lead to creation of action potential?

Smooth muscle from some sources displays spontaneous rhythmic activity and autonomic innervation influences contractility. In the gut interstitial cells of Cajal are specialized pacemaker cells. I'll read up on it. GetAgrippa 22:12, 20 November 2006 (UTC)


[edit] Fix-up

For being a member of two wikiprojects, this article shows poor composition and format. If someone would be able to clean it up, that would be great. The information is not structured with a focus on clean, informative text, but rather galloping ideas that skip over some significant points, such as the ones I added. DRosenbach (Talk | Contribs) 18:56, 23 July 2007 (UTC)

I agree. The article was a stub. I added to what was present by vomiting a bunch of information on the page touching on various subjects. The contraction relaxation info concentrates on cell signalling rather than biomechanics. A section on the biomechanical properties of various smooth muscle preparations would be interesting but probably overkill for an encyclopedia. Perhaps a secton of neurohumoral influences that effect smooth muscle containing tissues of the body-gut, skin goose bumps, erection, etc. This article doesn't generate much interest so I hadn't even bothered to add any references because I think much of what I added is probably not appropriate for an encyclopedia article anyways and will be removed. I had hoped someone familiar with this Wiki's format and experienced at writing encyclopedia articles would organize and rewrite it into something more useful. Subsections on cell signalling and biomechanics (stress-relaxation, hysteresis, shortening velocities of various tissues, etc.) might be appropriate. Perhaps a section on differences in proteins such as actin and myosin isoforms, lack of troponin and titin, significant other proteins like caldesmon and calponin, etc. Most of this Wiki's articles concerning muscle and contraction are poorly written and the emphasis is always vertebrate and particularly human rather than a general biological perspective that would encompass invertebrate and vertebrate. GetAgrippa 14:15, 24 July 2007 (UTC)
Hmm...I don't think that the focus of the article being human smooth muscle is at all a problem -- a quick survery of articles such as maxillary central incisor, gall bladder and trigeminal nerve all show a predominance of human anatomy and physiology over those of other species, vertebrate or not. This discussion has taken place at least in one place (hmmm...can't remember where exactly, but I know it had to do with the tooth article, in terms of "who" or "what" is the focus of our articles when it comes to multiple species and their possession of various anatomical and physiologic characteristics.)
I think the smooth muscle article should focus on the basics of smooth muscle anatomy and physiology, and discuss the differences of smooth in relation to skeletal and cardiac muscle.
I'll volunteer to redraft this article, if you give me two weeks or so. DRosenbach (Talk | Contribs) 02:09, 25 July 2007 (UTC)
The nomenclature used can be confusing and I noted on line searches yielded similar misinformation and confusion. Visceral smooth muscle can be multiunit or single unit. Including blood vessels with visceral smooth muscle is confusing as it is vascular smooth muscle. Smooth muscle from different visceral sources gut, etc. and from different areas of the vasculature are very different beast. I would think that an encyclopedia would be more general biology and not limited to vertebrate or human in its scope, and NPOV should encourage a more general article. I like your idea to compare skeletal, cardiac, and smooth muscle because that would bring up the topics of titin isoforms and stiffness (and the lack of titin in smooth muscle), the differences in shortening velocity-myosin isoforms and ADP affinity,etc, the lack of troponin in smooth muscle and calcium dependent MLC phosphorylation, differences in intracellular structure and content, differences in ionic channels. It could really make a nice separate article. In any case I am pleased you are willing to work on the article and I can assist in finding references for any given posit. Regards GetAgrippa 16:06, 25 July 2007 (UTC)

[edit] Advanced section

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)