- 関
- vascular smooth muscle cell
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出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2016/08/25 04:42:25」(JST)
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Diagram showing the location of vascular smooth muscle cells
Vascular smooth muscle cells, isolated from human aorta, growing and forming a monolayer in cell culture.
Vascular smooth muscle refers to the particular type of smooth muscle found within, and composing the majority of the wall of blood vessels.
Contents
- 1 Function
- 2 Innervation
- 3 See also
- 4 External links
Function
Vascular smooth muscle contracts or relaxes to change both the volume of blood vessels and the local blood pressure, a mechanism that is responsible for the redistribution of the blood within the body to areas where it is needed (i.e. areas with temporarily enhanced oxygen consumption). Thus the main function of vascular smooth muscle tone is to regulate the caliber of the blood vessels in the body. Excessive vasoconstriction leads to high blood pressure, while excessive vasodilation as in shock leads to low blood pressure.
Arteries have a great deal more smooth muscle within their walls than veins, thus their greater wall thickness. This is because they have to carry pumped blood away from the heart to all the organs and tissues that need the oxygenated blood. The endothelial lining of each is similar.
Innervation
Vascular smooth muscle is innervated primarily by the sympathetic nervous system through adrenergic receptors (adrenoceptors). Three types of adrenoceptors are present within vascular smooth muscle cells: , and . The main endogenous agonist of these cell receptors is norepinephrine (NE).
The adrenergic receptors exert opposite physiologic effects in the vascular smooth muscle under activation:
- receptors. Under NE binding receptors cause vasoconstriction (i.e. contraction of the vascular smooth muscle cells decreasing the diameter of the vessels). receptors are activated in response to shock or low blood pressure as a defensive reaction trying to restore the normal blood pressure. Antagonists of receptors (doxazosin, prazosin) cause vasodilation (i.e. decrease in vascular smooth muscle tone with increase of vessel diameter and decrease of the blood pressure). (See also receptor antagonist)
- receptors. Agonists of receptors in the vascular smooth muscle lead to vasoconstriction. However, in clinical practice drugs applied intravenously that are agonists of receptors (clonidine) lead to powerful vasodilation, which causes a decrease in blood pressure by presynaptic activation of receptors in the sympathetic ganglia. This presynaptic effect is predominant and completely overrides the vasoconstrictive effect of the receptors in the vascular smooth muscle.[citation needed]
- receptors. Agonism of receptors causes vasodilation and low blood pressure (i.e. the effect is opposite of the one resulting from activation of and receptors in the vascular smooth muscle cells). Usage of receptor agonists as hypotensive agents is less widespread due to adverse effects such as unnecessary bronchodilation in lungs and increase in blood sugar levels.
See also
External links
- Image of smooth muscle in the arterial walls
- Smooth muscle in stomach wall
Muscle tissue
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Smooth
muscle |
- Calmodulin
- Vascular smooth muscle
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Striated
muscle |
Skeletal
muscle |
Costamere/
DAPC |
Membrane/
extracellular |
DAP: |
- Sarcoglycan
- SGCA
- SGCB
- SGCD
- SGCE
- SGCG
- SGCZ
- Dystroglycan
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- Sarcospan
- Laminin, alpha 2
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Intracellular |
- Dystrophin
- Dystrobrevin
- Syntrophin
- Syncoilin
- Dysbindin
- Synemin/desmuslin
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related: |
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|
|
|
Sarcomere/
(a, i, and h bands;
z and m lines) |
- Myofilament
- thin filament/actin
- thick filament/myosin
- elastic filament/titin
- nebulin
|
|
Connective tissue |
- Epimysium
- Fascicle
- Perimysium
- Endomysium
- Connective tissue in skeletal muscle
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|
General |
- Neuromuscular junction
- Motor unit
- Muscle spindle
- Excitation–contraction coupling
- Sliding filament mechanism
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|
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Cardiac
muscle |
- Myocardium
- Intercalated disc
- Nebulette
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Both |
Fiber |
- Muscle fiber
- Myofibril
- Microfilament/Myofilament
- Sarcomere
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Cells |
- Myoblast/Myocyte
- Myosatellite cell
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Other |
- Desmin
- Sarcoplasm
- Sarcolemma
- Sarcoplasmic reticulum
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|
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Other/
ungrouped |
- Myotilin
- Telethonin
- Dysferlin
- Fukutin
- Fukutin-related protein
|
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UpToDate Contents
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English Journal
- Myocyte Enhancer Factor 2A Regulates Hydrogen Peroxide-Induced Senescence of Vascular Smooth Muscle Cells Via microRNA-143.
- Zhao W1, Zheng XL2, Peng DQ1, Zhao SP1.
- Journal of cellular physiology.J Cell Physiol.2015 Sep;230(9):2202-11. doi: 10.1002/jcp.24948.
- Myocyte enhancer factor 2A (MEF2A) is involved in vascular smooth muscle cell (VSMC) proliferation, migration, and senescence. MicroRNA-143/145 (miR-143/145), which may be regulated by MEF2A, is known to promote cellular senescence. We hypothesized that MEF2A may promote VSMC senescence via miR-143/
- PMID 25655189
- TIPE2 protein prevents injury-induced restenosis in mice.
- Zhang G1, Zhao L2, Wang Y1, Shao J1, Cui J1, Lou Y1, Geng M1, Zhang N1, Chen YH3, Liu S4.
- Biochimica et biophysica acta.Biochim Biophys Acta.2015 Aug;1852(8):1574-84. doi: 10.1016/j.bbadis.2015.04.018. Epub 2015 Apr 22.
- Proliferation of vascular smooth muscle cells (VSMCs) plays an important role in restenosis, a disease characterized by smooth muscle cell hyperplasia and neointimal formation. How proliferation signals are controlled to avoid restenosis is not fully understood. Here we report that TIPE2, the tumor
- PMID 25912734
- Cell compatibility of a maghemite/polymer biomedical nanoplatform.
- Ali LM1, Piñol R2, Villa-Bellosta R3, Gabilondo L2, Millán A4, Palacio F5, Sorribas V6.
- Toxicology in vitro : an international journal published in association with BIBRA.Toxicol In Vitro.2015 Aug;29(5):962-75. doi: 10.1016/j.tiv.2015.04.003. Epub 2015 Apr 16.
- We are reporting the cytocompatibility and cellular fate of an iron oxide/polymer nanoplatform (IONP) in its most basic formulation, using both mesenchymal (vascular smooth muscle cells, VSMC), and epithelial (opossum kidney, OK) cells. The cytotoxicity and cell internalization of the nanoplatform h
- PMID 25891827
Japanese Journal
- Elongation of Long‐Chain Fatty Acid Family Member 6 (Elovl6)‐Driven Fatty Acid Metabolism Regulates Vascular Smooth Muscle Cell Phenotype Through AMP‐Activated Protein Kinase/Krüppel‐Like Factor 4 (AMPK/KLF4) Signaling
- 血管傷害後内膜肥厚形成段階の血管平滑筋細胞アポトーシスにおけるKeap1/Nrf2システムの役割
- The vascular clock system generates the intrinsic circadian rhythm of vascular contractility
Related Links
- 型式選択 チェック 型式 仕様 1.基本型式 VSMC φ81 2設定出力・4~20mA出力搭載 丸形デジタル圧力計 2.センサ接続方法 AS センサ下付き直結ツバ無し 3.アナログ出力 3 4~20mA 4.設定出力数 2P 2点フォトモスリレーa接点出力
- サービスを試すにあたって、まずはVSMC上にアプリを作成する必要があります。 サインインページにアクセスして、 「Connect with Github」をクリックします。 Githubにサインインします。 OAuthの認可画面が表示されるので「Authorize ...
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