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| [[File:Endotelijalna ćelija.jpg|thumb|350px||right|Diagram showing the location of vascular smooth muscle cells]]
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| [[Image:Human_Aortic_SMC.jpg|thumb|350px|right|Vascular smooth muscle cells, isolated from human aorta, growing and forming a monolayer in cell culture.]]
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| '''Vascular smooth muscle''' refers to the particular type of [[smooth muscle]] found within, and composing the majority of the wall of [[blood vessel]]s.
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| ==Function==
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| 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]].
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| [[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.
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| ==Innervation==
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| 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).
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| The adrenergic receptors exert opposite physiologic effects in the vascular smooth muscle under activation:
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| * '''<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]])
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| * '''<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}}
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| * '''<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.
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| ==See also==
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| * [[Mural cell]]
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| ==External links==
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| * [http://www.ii.bham.ac.uk/clinicalimmunology/CISimagelibrary/smoothmuscle.htm Image of smooth muscle in the arterial walls]
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| * [http://www.antibodypatterns.com/smoothmuscle.php Smooth muscle in stomach wall]
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| {{Muscle tissue}}
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| [[Category:Angiology]]
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