Arteriole

Source: Wikipedia, the free encyclopedia.
Arteriole
Types of blood vessels, including an arteriole and artery, as well as capillaries.
Rabbit arteriole at 100X
Details
Pronunciation/ɑːrˈtɪəri.oʊl/
Identifiers
Latinarteriola
MeSHD001160
TA98A12.0.00.005
TA23900
FMA63182
Anatomical terminology

An arteriole is a small-diameter blood vessel in the microcirculation that extends and branches out from an artery and leads to capillaries.[1]

Arterioles have

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

gap junctions
between the endothelial cells and the vascular smooth muscle.

Physiology

Blood pressure

total peripheral resistance. An increase in the tunica 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 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

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.

Arteriosclerosis

Main article: Arteriosclerosis

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

Main article:
autoimmune response.

Medication

The muscular contraction of arterioles is targeted by drugs that lower blood pressure (

dihydropyridines (nifedipine and nicardipine), which block the calcium conductance
in the muscular layer of the arterioles, causing relaxation.

This decreases the resistance to flow into peripheral vascular beds, lowering overall systemic pressure.

Metarterioles

A "metarteriole" is an arteriole which bypasses capillary circulation.[7]

See also

This article uses anatomical terminology.

References

  1. ISBN 0-13-981176-1
    .
  2. PMID 32310381
    . Retrieved 17 November 2022.
  3. PMID 2947873
    .
  4. ^ 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
  5. PMID 21152417
    .
  6. PMID 23777785. Archived from the original
    on 2013-11-02. Retrieved 2013-06-26.
  7. ^ Nosek, Thomas M. "Section 3/3ch9/s3ch9_2". Essentials of Human Physiology. Archived from the original on 2016-03-24.
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