| Arteriole | |
|---|---|
 Types of blood vessels, including an arteriole and artery, as well as capillaries. | |
 Rabbit arteriole at 100X | |
| Details | |
| Pronunciation | /ɑːrˈtɪəri.oʊl/ |
| Identifiers | |
| Latin | arteriola |
| MeSH | D001160 |
| TA98 | A12.0.00.005 |
| TA2 | 3900 |
| FMA | 63182 |
| Anatomical terminology | |
Anarteriole is a small-diameterblood vessel in themicrocirculation that extends and branches out from anartery and leads tocapillaries.[1]
Arterioles havemuscular walls (usually only one to two layers ofsmooth muscle cells) and are the primary site ofvascular 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]
In a healthy vascular system, theendothelium lines all blood-contacting surfaces, including arteries, arterioles, veins, venules, capillaries, and heart chambers. This healthy condition is promoted by the ample production ofnitric oxide by the endothelium, which requires a biochemical reaction regulated by a complex balance ofpolyphenols, variousnitric oxide synthaseenzymes and L-arginine. In addition, there is direct electrical and chemical communication viagap junctions between the endothelial cells and the vascular smooth muscle.
Blood pressure in the arteries supplying the body is a result of the work needed to pump thecardiac output (the flow of blood pumped by the heart) through thevascular resistance, sometimes termedtotal peripheral resistance. An increase in thetunica media to luminal diameter ratio has been observed in hypertensive arterioles (arteriolosclerosis) as the vascular wall thickens and/or luminal diameter decreases.
The up and down fluctuation of thearterial blood pressure is due to the pulsatile nature of thecardiac output and determined by the interaction of thestroke volume versus the volume and elasticity of the major arteries.
The decreased velocity of flow in the capillaries increases the blood pressure, due toBernoulli's principle. This induces gas and nutrients to move from the blood to the cells, due to the lowerosmotic pressure outside the capillary. The opposite process occurs when the blood leaves the capillaries and enters thevenules, where the blood pressure drops due to an increase in flow rate. Arterioles receiveautonomic nervous system innervation and respond to various circulatinghormones in order to regulate their diameter. Retinal vessels lack a functional sympathetic innervation.[3]
Arteriole diameter varies according to autoregulation of organs or tissues to maintain sufficient blood flow despite changes in pressure via metabolic ormyogenic 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).
Arteriole diameters decrease with age and with exposure toair pollution.[5][6]
Any pathology which constricts blood flow, such asstenosis, will increase total peripheral resistance and lead tohypertension.
Arteriolosclerosis is the term specifically used for the hardening of arteriole walls. This can be due to decreased elastic production from fibrinogen, associated withageing, orhypertension or pathological conditions such asatherosclerosis.
Arteritis of the arterioles occurs when the arteriole walls becomeinflamed as a result of either an immune response to infection or anautoimmune response.
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The muscular contraction of arterioles is targeted by drugs that lower blood pressure (antihypertensives), for example thedihydropyridines (nifedipine andnicardipine), which block thecalcium conductance in the muscular layer of the arterioles, causing relaxation.
This decreases the resistance to flow into peripheral vascular beds, lowering overall systemic pressure.
A "metarteriole" is an arteriole which bypasses capillary circulation.[7]
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