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.

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: $\alpha_1$ , $\alpha_2$ 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 drugs applied intravenously that are agonists of $\alpha_2$ receptors (clonidine) lead to powerful vasodilation, which causes a decrease in 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 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.

External links

Histology: muscle tissue (TH H2.00.05, H3.3)

Smooth
muscle

Striated
muscle

Skeletal
muscle

Costamere/
DAPC

Membrane/
extracellular

DAP:	Sarcoglycan SGCA SGCB SGCD SGCE SGCG SGCZ Dystroglycan

Sarcospan Laminin, alpha 2

Intracellular

Dystrophin Dystrobrevin A B Syntrophin A B1 B2 G1 G2 Syncoilin Dysbindin Synemin/desmuslin

related:	NOS1 Caveolin 3

Sarcomere/
(a, i, and h bands;
z and m lines)

Myofilament

Tropomyosin

Troponin
- T
- C
- I

Connective tissue

General

Cardiac
muscle

Both

Fiber	Muscle fiber intrafusal extrafusal Myofibril Microfilament/Myofilament Sarcomere

Cells	Myoblast/Myocyte Myosatellite cell

Other	Desmin Sarcoplasm Sarcolemma T-tubule Sarcoplasmic reticulum

Other/
ungrouped

This article is issued from Wikipedia - version of the Wednesday, February 03, 2016. The text is available under the Creative Commons Attribution/Share Alike but additional terms may apply for the media files.

Vascular smooth muscle

Function

Innervation

See also

External links