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Vascular smooth muscle

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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.

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

Contents

  • Function 1
  • Innervation 2
  • See also 3
  • External links 4

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 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.

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: \alpha_1, \alpha_2 and \beta_2. 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 i.e. contraction of the vascular smooth muscle cells decreasing the diameter of the vessels. \alpha_1 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 i.e. 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 applied intravenously drugs being agonists of \alpha_2 receptors (clonidine) leads to powerful vasodilation and decrease in the blood pressure by presynaptic activation of \alpha_2 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.
  • \beta_2 receptors. Agonism at \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 agonists of \beta_2 receptors 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
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