Arterioles have muscular walls (usually only one to two layers of smooth muscle cells) and are the primary site of vascular resistance. The greatest change in blood pressure and velocity of blood flow occurs at the transition of arterioles to capillaries. This function is extremely important because it prevents the thin, one-layer capillaries from exploding upon pressure. The arterioles achieve this decrease in pressure, as they are the site with the highest resistance (a large contributor to total peripheral resistance) which translates to a large decrease in the pressure.[2]
Structure
Microanatomy
In a healthy vascular system the endothelium lines all blood-contacting surfaces, including arteries, arterioles, veins, venules, capillaries, and heart chambers. This healthy condition is promoted by the ample production of nitric oxide by the endothelium, which requires a biochemical reaction regulated by a complex balance of polyphenols, various nitric oxide synthaseenzymes and L-arginine. In addition there is direct electrical and chemical communication via gap junctions between the endothelial cells and the vascular smooth muscle.
The up and down fluctuation of the arterial blood pressure is due to the pulsatile nature of the cardiac output and determined by the interaction of the stroke volume versus the volume and elasticity of the major arteries.
The decreased velocity of flow in the capillaries increases the blood pressure, due to Bernoulli's principle. This induces gas and nutrients to move from the blood to the cells, due to the lower osmotic pressure outside the capillary. The opposite process occurs when the blood leaves the capillaries and enters the venules, where the blood pressure drops due to an increase in flow rate. Arterioles receive autonomic nervous system innervation and respond to various circulating hormones in order to regulate their diameter. Retinal vessels lack a functional sympathetic innervation.[3]
Autoregulation
Arteriole diameter varies according to autoregulation of organs or tissues to maintain sufficient blood flow despite changes in pressure via metabolic or myogenic factors which include stretch, carbon dioxide, and oxygen among other factors.[4] Generally, norepinephrine and epinephrine (hormones produced by sympathetic nerves and the adrenal gland medulla) are vasoconstrictive acting on alpha 1-adrenergic receptors. However, the arterioles of skeletal muscle, cardiac muscle, and pulmonary circulation vasodilate in response to these hormones when they act on beta-adrenergic receptors. Generally, stretch and high oxygen tension increase tone, and carbon dioxide and low pH promote vasodilation. Pulmonary arterioles are a noteworthy exception as they vasodilate in response to high oxygen. Brain arterioles are particularly sensitive to pH with reduced pH promoting vasodilation. A number of hormones influence arteriole tone such as angiotensin II (vasoconstrictive), endothelin (vasoconstrictive), bradykinin (vasodilation), atrial natriuretic peptide (vasodilation), and prostacyclin (vasodilation).
Clinical significance
Arteriole diameters decrease with age and with exposure to air pollution.[5][6]
Disease
Decreased diameter of Arteriole.
Any pathology which constricts blood flow, such as stenosis, will increase total peripheral resistance and lead to hypertension.
Arteriolosclerosis is the term specifically used for the hardening of arteriole walls. This can be due to decreased elastic production from fibrinogen, associated with ageing, or hypertension or pathological conditions such as atherosclerosis.
Arteritis of the arterioles occurs when the arteriole walls become inflamed as a result of either an immune response to infection or an autoimmune response.
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^Maton, Anthea; Jean Hopkins; Charles William McLaughlin; Susan Johnson; Maryanna Quon Warner; David LaHart; Jill D. Wright (1993). Human Biology and Health. Englewood Cliffs, New Jersey: Prentice Hall. ISBN0-13-981176-1.
^Rahman, Masum; Abu Bakar, Siddik (4 December 2021). StatPearls [Internet] (Updated ed.). Treasure Island (FL): StatPearls Publishing. pp. 2–5. PMID32310381. Retrieved 17 November 2022.
^Riva, CE; Grunwald, JE; Petrig, BL (1986). "Autoregulation of human retinal blood flow. An investigation with laser Doppler velocimetry". Invest Ophthalmol Vis Sci. 27 (12): 1706–1712. PMID2947873.
^Johnson, P. C. (1986). Autoregulation of blood flow. In Circulation Research (Vol. 59, Issue 5, pp. 483–495). Ovid Technologies (Wolters Kluwer Health). https://doi.org/10.1161/01.res.59.5.483
