Vascular smooth muscle: Difference between revisions

Vascular smooth muscle
Vascular smooth muscle
	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.
Details
Part of	smooth muscle wall of blood vessels
Identifiers
MeSH	D009131
	Anatomical terminology [edit on Wikidata]

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Vascular smooth muscle is the type of smooth muscle that makes up most of the walls of blood vessels.

Structure

Vascular smooth muscle refers to the particular type of smooth muscle found within, and composing the majority of the wall of blood vessels.

Nerve supply

Vascular smooth muscle is innervated primarily by the sympathetic nervous system through adrenergic receptors (adrenoceptors). The three types present are: alpha-1, alpha-2 and beta-2 adrenergic receptors|. 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:

alpha-1 receptors. Under NE binding alpha-1 receptors cause vasoconstriction (contraction of the vascular smooth muscle cells decreasing the diameter of the vessels). These receptors are activated in response to shock or low blood pressure as a defensive reaction trying to restore the normal blood pressure. Antagonists of alpha-1 receptors (doxazosin, prazosin) cause vasodilation (a decrease in vascular smooth muscle tone with increase of vessel diameter and decrease of the blood pressure). (See also receptor antagonist)
alpha-2 receptors. Agonists of alpha-2 receptors in the vascular smooth muscle lead to vasoconstriction. However, in clinical practice drugs applied intravenously that are agonists of alpha-2 receptors such as clonidine lead to powerful vasodilation, which causes a decrease in blood pressure by presynaptic activation of the receptors in the sympathetic ganglia. This presynaptic effect is predominant and completely overrides the vasoconstrictive effect of the alpha-2 receptors in the vascular smooth muscle.^{[citation needed]}
beta-2 receptors. Agonism of beta-2 receptors causes vasodilation and low blood pressure (i.e. the effect is opposite of the one resulting from activation of alpha-1 and alpha-2 receptors in the vascular smooth muscle cells). Usage of beta-2 receptor agonists as hypotensive agents is less widespread due to adverse effects such as unnecessary bronchodilation in lungs and increase in blood sugar levels.

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. Vascular smooth muscle cells also play important roles during development, e.g. driving osteocyte differentiation from undifferentiated precursors during osteogenesis ^[1].

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.

Excessive proliferation of vascular smooth muscle cells contributes to the progression of pathological conditions, such as vascular inflammation, plaque formation, atherosclerosis, restenosis, and pulmonary hypertension.^[2]^[3] Recent studies have shown that the majority of cells within atherosclerotic plaque, the predominant cause of heart attack and stroke, are vascular smooth muscle cell derived.^[4]

References

^ Fernandes CJ, Silva RA, Ferreira MR, Fuhler GM, Peppelenbosch MP, van der Eerden BC, Zambuzzi WF (August 2024). "Vascular smooth muscle cell-derived exosomes promote osteoblast-to-osteocyte transition via β-catenin signaling". Experimental Cell Research. 442: 114211. doi:10.1016/j.yexcr.2024.114211. PMID 39147261.
^ Bennett, M. R; Sinha, S; Owens, G. K (2016). "Vascular smooth muscle cells in atherosclerosis". Circulation Research. 118 (4): 692–702. doi:10.1161/CIRCRESAHA.115.306361. PMC 4762053. PMID 26892967.
^ Wang, D; Uhrin, P; Mocan, A; Waltenberger, B; Breuss, J. M; Tewari, D; Mihaly-Bison, J; Huminiecki, Łukasz; Starzyński, R. R; Tzvetkov, N. T; Horbańczuk, J; Atanasov, A. G (2018). "Vascular smooth muscle cell proliferation as a therapeutic target. Part 1: Molecular targets and pathways". Biotechnology Advances. 36 (6): 1586–1607. doi:10.1016/j.biotechadv.2018.04.006. PMID 29684502.
^ Harman, Jennifer L.; Jørgensen, Helle F. (October 2019). "The role of smooth muscle cells in plaque stability: Therapeutic targeting potential". British Journal of Pharmacology. 176 (19): 3741–3753. doi:10.1111/bph.14779. ISSN 0007-1188. PMC 6780045. PMID 31254285.

External links

[1] Fernandes CJ, Silva RA, Ferreira MR, Fuhler GM, Peppelenbosch MP, van der Eerden BC, Zambuzzi WF (August 2024). "Vascular smooth muscle cell-derived exosomes promote osteoblast-to-osteocyte transition via β-catenin signaling". Experimental Cell Research. 442: 114211. doi:10.1016/j.yexcr.2024.114211. PMID 39147261.

[2] Bennett, M. R; Sinha, S; Owens, G. K (2016). "Vascular smooth muscle cells in atherosclerosis". Circulation Research. 118 (4): 692–702. doi:10.1161/CIRCRESAHA.115.306361. PMC 4762053. PMID 26892967.

[3] Wang, D; Uhrin, P; Mocan, A; Waltenberger, B; Breuss, J. M; Tewari, D; Mihaly-Bison, J; Huminiecki, Łukasz; Starzyński, R. R; Tzvetkov, N. T; Horbańczuk, J; Atanasov, A. G (2018). "Vascular smooth muscle cell proliferation as a therapeutic target. Part 1: Molecular targets and pathways". Biotechnology Advances. 36 (6): 1586–1607. doi:10.1016/j.biotechadv.2018.04.006. PMID 29684502.

[4] Harman, Jennifer L.; Jørgensen, Helle F. (October 2019). "The role of smooth muscle cells in plaque stability: Therapeutic targeting potential". British Journal of Pharmacology. 176 (19): 3741–3753. doi:10.1111/bph.14779. ISSN 0007-1188. PMC 6780045. PMID 31254285.

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@@ Line 1: / Line 1: @@
+{{Short description|Smooth muscle tissue in the walls of blood vessels}}
-[[File:Endotelijalna ćelija.jpg|thumb|350px||right|Diagram showing the location of vascular smooth muscle cells]]
+{{Infobox anatomy
-[[Image:Human_Aortic_SMC.jpg|thumb|350px|right|Vascular smooth muscle cells, isolated from human aorta, growing and forming a monolayer in cell culture.]]
+| Name        = Vascular smooth muscle
-'''Vascular smooth muscle''' refers to the particular type of [[smooth muscle]] found within, and composing the majority of the wall of [[blood vessel]]s.
+| Latin       =
+| Image       = Endotelijalna ćelija.jpg
+| Caption     = Diagram showing the location of vascular smooth muscle cells.
+| Image2      = Human_Aortic_SMC.jpg
+| Caption2    = Vascular smooth muscle cells, isolated from human aorta, growing and forming a monolayer in cell culture.
+| Width       =
+| Precursor   =
+| System      =
+| Artery      =
+| Vein        =
+| Part_of     = [[smooth muscle]] wall of [[blood vessel]]s
+| Nerve       =
+| Lymph       =
+}}
+'''Vascular smooth muscle''' is the type of [[smooth muscle]] that makes up most of the walls of [[blood vessel]]s.
-==Function==
-Vascular smooth muscle contracts or relaxes to both change 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 tonus]] is to regulate the caliber of the blood vessels in the body. Excessive [[vasoconstriction]] leads to [[hypertension]], while excessive [[vasodilation]] as in shock leads to [[hypotension]].
+==Structure==
-[[Artery|Arteries]] have a great deal more [[smooth muscle]] within their walls than [[vein]]s, 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 [[endothelium|endothelial]] lining of each is similar.
+Vascular smooth muscle refers to the particular type of [[smooth muscle]] found within, and composing the majority of the wall of [[blood vessel]]s.
-==Innervation==
+===Nerve supply===
-Vascular smooth muscle is innervated primarily by the [[sympathetic nervous system]] through [[adrenergic receptor]]s (adrenoceptors). Three types of [[adrenoceptor]]s are present within vascular smooth muscle cells: <math>\alpha_1</math>, <math>\alpha_2</math> and <math>\beta_2</math>. The main endogenous agonist of these cell receptors is [[norepinephrine]] (NE).
+Vascular smooth muscle is innervated primarily by the [[sympathetic nervous system]] through [[adrenergic receptor]]s (adrenoceptors). The three types present are: [[Alpha-1 adrenergic receptor|alpha-1]], [[Alpha-2 adrenergic receptor|alpha-2]] and [[beta-2 adrenergic receptor]]s|. The main [[endogeny|endogenous]] [[agonist]] of these cell receptors is [[norepinephrine]] (NE).
 The adrenergic receptors exert opposite physiologic effects in the vascular smooth muscle under activation:
-* '''<math>\alpha_1</math> ''receptors'''''. Under NE binding <math>\alpha_1</math> receptors cause [[vasoconstriction]] i.e. contraction of the vascular smooth muscle cells decreasing the diameter of the vessels. <math>\alpha_1</math> receptors are activated in response to shock or hypotension as a defensive reaction trying to restore the normal blood pressure. Antagonists of <math>\alpha_1</math> 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]])
+* '''alpha-1 receptors'''. Under NE binding alpha-1 receptors cause [[vasoconstriction]] (contraction of the vascular smooth muscle cells decreasing the diameter of the vessels). These receptors are activated in response to shock or low blood pressure as a defensive reaction trying to restore the normal blood pressure. Antagonists of alpha-1 receptors ([[doxazosin]], [[prazosin]]) cause [[vasodilation]] (a decrease in vascular smooth muscle tone with increase of vessel diameter and decrease of the blood pressure). (See also [[receptor antagonist]])
+* '''alpha-2 receptors'''. [[Agonist]]s of alpha-2 receptors in the vascular smooth muscle lead to vasoconstriction. However, in clinical practice drugs applied intravenously that are agonists of alpha-2 receptors such as [[clonidine]] lead to powerful vasodilation, which causes a decrease in blood pressure by presynaptic activation of the receptors in the sympathetic ganglia. This presynaptic effect is predominant and completely overrides the vasoconstrictive effect of the alpha-2 receptors in the vascular smooth muscle.{{Citation needed|date=December 2009}}
+* '''beta-2 receptors'''. Agonism of beta-2 receptors causes [[vasodilation]] and [[hypotension|low blood pressure]] (i.e. the effect is opposite of the one resulting from activation of alpha-1 and alpha-2 receptors in the vascular smooth muscle cells). Usage of beta-2 receptor agonists as hypotensive agents is less widespread due to adverse effects such as unnecessary [[bronchodilator|bronchodilation]] in lungs and increase in [[blood sugar]] levels.
+==Function==
-* '''<math>\alpha_2</math> ''receptors'''''. [[Agonist]]s of <math>\alpha_2</math> receptors in the vascular smooth muscle lead to vasoconstriction. However, in clinical practice applied intravenously drugs being agonists of <math>\alpha_2</math> receptors ([[clonidine]]) leads to powerful vasodilation and decrease in the blood pressure by presynaptic activation of  <math>\alpha_2</math> receptors in the sympathetic ganglia. This presynaptic effect is predominant and completely overrides the vasoconstrictive effect of the <math>\alpha_2</math> receptors in the vascular smooth muscle.{{Citation needed|date=December 2009}}
+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 [[hypertension|high blood pressure]], while excessive [[vasodilation]] as in shock leads to [[hypotension|low blood pressure]]. Vascular smooth muscle cells also play important roles during development, e.g. driving osteocyte differentiation from undifferentiated precursors during [[osteogenesis]] <ref> {{cite journal | vauthors = Fernandes CJ, Silva RA, Ferreira MR, Fuhler GM, Peppelenbosch MP, van der Eerden BC, Zambuzzi WF| title = Vascular smooth muscle cell-derived exosomes promote osteoblast-to-osteocyte transition via β-catenin signaling. | journal =  Experimental Cell Research | volume = 442  | pages = 114211| date = August 2024 | pmid = 39147261| doi = 10.1016/j.yexcr.2024.114211 }}</ref>.
-* '''<math>\beta_2</math> ''receptors'''''. Agonism at <math>\beta_2</math> receptors causes [[vasodilation]] and [[hypotension]], i.e. the effect is opposite of the one resulting from activation of <math>\alpha_1</math> and <math>\alpha_2</math> receptors in the vascular smooth muscle cells. Usage of agonists of <math>\beta_2</math> receptors as hypotensive agents is less widespread due to adverse effects such as unnecessary [[bronchodilator |bronchodilation]] in lungs and increase in [[blood sugar]] levels.
+[[Artery|Arteries]] have a great deal more [[smooth muscle]] within their walls than [[vein]]s, 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 [[endothelium|endothelial]] lining of each is similar.
+Excessive proliferation of vascular smooth muscle cells contributes to the progression of pathological conditions, such as vascular [[inflammation]], [[Sclerosis (medicine)|plaque formation]], [[atherosclerosis]], [[restenosis]], and [[pulmonary hypertension]].<ref>{{cite journal|pmc=4762053|year=2016|last1=Bennett|first1=M. R|title=Vascular smooth muscle cells in atherosclerosis|journal=Circulation Research|volume=118|issue=4|pages=692–702|last2=Sinha|first2=S|last3=Owens|first3=G. K|doi=10.1161/CIRCRESAHA.115.306361|pmid=26892967}}</ref><ref>{{cite journal|pmid=29684502|year=2018|last1=Wang|first1=D|title=Vascular smooth muscle cell proliferation as a therapeutic target. Part 1: Molecular targets and pathways|journal=Biotechnology Advances|last2=Uhrin|first2=P|last3=Mocan|first3=A|last4=Waltenberger|first4=B|last5=Breuss|first5=J. M|last6=Tewari|first6=D|last7=Mihaly-Bison|first7=J|last8=Huminiecki|first8=Łukasz|last9=Starzyński|first9=R. R|last10=Tzvetkov|first10=N. T|last11=Horbańczuk|first11=J|last12=Atanasov|first12=A. G|volume=36|issue=6|pages=1586–1607|doi=10.1016/j.biotechadv.2018.04.006}}</ref> Recent studies have shown that the majority of cells within [[Atheroma|atherosclerotic plaque]], the predominant cause of [[Myocardial infarction|heart attack]] and [[stroke]], are vascular smooth muscle cell derived.<ref>{{Cite journal|last=Harman|first=Jennifer L.|last2=Jørgensen|first2=Helle F.|date=October 2019|title=The role of smooth muscle cells in plaque stability: Therapeutic targeting potential|journal=British Journal of Pharmacology|language=en|volume=176|issue=19|pages=3741–3753|doi=10.1111/bph.14779|issn=0007-1188|pmc=6780045|pmid=31254285}}</ref>
 ==See also==
 * [[Mural cell]]
+==References==
+{{reflist|30em}}
 ==External links==