Vascular smooth muscle

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Human Vascular smooth muscle isolated from Aorta

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]



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

Vascular smooth muscle contracts or relaxes to both change the volume of blood vessels and the local blood pressure, a mechanism that is responsible to 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.

Arteries have a great deal more smooth muscle within their walls than veins, thus their greater wall thickness. This is because they have to pump blood away from the heart to all the organs and tissues that need the oxygenated blood. The endothelial lining of each is similar.

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: α1, α2 and β2. 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:

  • α1 receptors. Under NE binding α1 receptors cause vasoconstriction i.e. contraction of the vascular smooth muscle cells decreasing the diameter of the vessels. α1 receptors are activated in response to shock or hypotension as a defensive reaction trying to restore the normal blood pressure. Antagonists of α1 receptors (doxazosin, prazosin) cause vasodilation i.e. decrease in vascular smooth muscle tone with increase of vessel dimater and decrease of the blood pressure. (See also receptor antagonist)
  • α2 receptors. Agonists of α2 receptors in the vascular smooth muscle lead to vasoconstriction. However in clinical practice applied intravenously drugs being agonists of α2 receptors (chlophazolin) leads to powerful vasodilation and decrease in the blood pressure by presynaptic activation of α2 receptors in the sympathetic ganglia. This presynaptic effect is predominant and completely overrides the vasoconstrictive effect of the α2 receptors in the vascular smooth muscle.
  • β2 receptors. Agonism at β2 receptors causes vasodilation and hypotension, i.e. the effect is opposite of the one resulting from activation of α1 and α2 receptors in the vascular smooth muscle cells. Usage of agonists of β2 receptors as hypotensive agents is less widespread due to adverse effects such as unnecessary bronchodilation in lungs and increase in blood sugar levels.

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