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Carotid body
Section of part of human glomus caroticum. Highly magnified. Numerous bloodvessels are seen in section among the gland cells.
Latin glomus caroticum
Gray's subject #277 1281
MeSH [1]
Diagram showing the origins of the main branches of the carotid arteries.

The carotid body (or carotid glomus) is a small cluster of chemoreceptors and supporting cells located near the bifurcation of the carotid artery.

It measures changes in the composition of arterial blood flowing through it, mainly the partial pressure of oxygen, but also of carbon dioxide. Furthermore, it is also sensitive to changes in pH and temperature.


The carotid body is made up of two types of cell: type I (glomus) cells, and type II (sustentacular) cells. Glomus cells are derived from neural crest,[1] which, in turn are derived from neuroectoderm. They release a variety of neurotransmitters, including acetylcholine, ATP, and dopamine that trigger EPSP's in synapsed neurons leading to the respiratory center.

Type II cells resemble glia and act as supporting cells.


The carotis body functions by a stimulus, in this case mainly O2 partial pressure, is detected by the type I (glomus) cells, and triggers an action potential in an afferent nerve fiber, which relays the information to the central nervous system.


While the central chemoreceptors in the brainstem are highly sensitive to CO2 the carotid body is a peripheral chemoreceptor that mainly provides afferent input to the respiratory center that is highly O2 dependent. However, the carotid body also senses increases in CO2 partial pressure and decreases in arterial pH, but to a lesser degree than for O2

The output of the carotid bodies is low at an oxygen partial pressure above about 100 mmHg (torr) (at normal physiological pH), but below this the activity of the type I (glomus) cells increases rapidly.


The mechanism for detecting reductions in PO2 is not well understood. There may be a heme-containing protein in the glomus cell which responds to the loss of complexed oxygen by reducing the probability of potassium channels being open. Another possibility is that low PO2 inhibits NADPH oxidase in mitochondria. This would increase the ratio of reduced glutathione to oxidised glutathione, which blocks potassium channels.

An increased PCO2 is detected because the CO2 diffuses into the cell, where it increase the concentration of carbonic acid and thus protons. These protons displace calcium from high-conductance calcium channels, reducing potassium current.

Arterial acidosis (either metabolic or from altered PCO2) inhibits acid-base transporters (e.g. Na+-H+) which raise intracellular pH, and activates transporters (e.g. Cl--HCO3-) which decrease it. Changes in proton concentration caused by acidosis (or the opposite from alkalosis) inside the cell stimulates the same pathways involved in PCO2 sensing.

Action potential

The type 1 (glomus) cells in the carotid (and aortic bodies) are derived from neuroectoderm and are thus electrically excitable. A decrease in oxygen partial pressure, an increase in carbon dioxide partial pressure, and a decrease in arterial pH can all cause depolarization of the cell membrane, and they effect this by blocking potassium currents. This reduction in the membrane potential opens voltage-gated calcium channels, which causes a rise in intracellular calcium concentration. This causes exocytosis of vesicles containing a variety of neurotransmitters, including acetylcholine, noradrenaline, dopamine, substance P, and met-enkephalin. These act on receptors on the afferent nerve fibres which lie in apposition to the glomus cell to cause an action potential.


The feedback from the carotid body is sent to the respiratory centers in the medulla oblongata via the afferent branches of the glossopharyngeal nerve (IX). These centers, in turn, regulate breathing and blood pressure.


A paraganglioma is a tumor that may involve the carotid body.


  1. Gonzalez C, Almaraz L, Obeso A, Rigual R (1994). Carotid body chemoreceptors: from natural stimuli to sensory discharges. Physiol. Rev. 74 (4): 829–98.

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