carotid body

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

The carotid body (carotid glomus or glomus caroticum) is a small cluster of chemoreceptors and supporting cells located near the fork (bifurcation) of the carotid artery (which runs along both sides of the throat).

The carotid body detects 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.

Composition

The carotid body is made up of two types of cells, called glomus cells: glomus type I (chief) cells, and glomus type II (sustentacular) cells.

• Glomus type I/chief 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 EPSPs in synapsed neurons leading to the respiratory center.

• Glomus type II/sustentacular cells resemble glia, express the glial marker S100 and act as supporting cells.

Function

The carotid body functions as a sensor, it responds to a stimulus, primarily O₂ partial pressure, which is detected by the type I (glomus) cells, and triggers an action potential in an afferent nerve fiber, the carotid sinus nerve, which relays the information to the central nervous system.

Stimulus

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 (13,3 kPa) (at normal physiological pH), but below this the activity of the type I (glomus) cells increases rapidly.

Detection

The mechanism for detecting reductions in PO₂ is not well understood. No one single hypoxia sensor has yet been definitively identified, and it will likely vary to some extent between species. The possibility that more than one hypoxia sensor is involved cannot be ruled out ^[2]. There are a number of conflicting hypotheses regarding the manner in which oxygen is sensed. The first of these hypotheses involved mitochondrial oxygen sensors, specifically it suggests a role for the haem-containing cytochromes that undergo reversible one-electron reduction during oxidative-phosphorylation. Haem reversibly binds O₂ with an affinity similar to that of the carotid body, suggesting that haem containing proteins may have a role in O₂, potentially this could be one of the complexes involved in oxidative-phosphorylation. It is thought that this leads to increases in reactive oxygen species and initiate rises in intracellular Ca²⁺. However, there is currently no consensus on whether hypoxia leads to an increase or decrease in reactive oxygen species. The role of reactive oxygen species in hypoxia sensing is also under question ^[3]. The oxygen dependent enzyme haem-oxidase has also been put forward as a hypoxia sensor. In normoxia, haem-oxygenase generates carbon monoxide (CO), CO activates the large conductance calcium-activated potassium channel, BK. Falls in CO that occur as a consequence of hypoxia would lead to closure of this potassium channel and this would lead to membrane depolarisation and consequence activation of the carotid body ^[4]. A role for the "energy sensor" AMP-activated protein kinase (AMPK) has also been proposed in hypoxia sensing. This enzyme is activated during times of net energy usage and metabolic stress, including hypoxia. AMPK has a number of targets and it appears that, in the carotid body, when AMPK is activated by hypoxia, it leads to downstream potassium channel closure of both O₂-sentive TASK-like and BK channels ^[5]

An increased PCO₂ is detected because the CO₂ diffuses into the cell, where it increases the concentration of carbonic acid and thus protons. The precise mechanism of CO₂ sensing is unknown, however it has been demonstrated that CO₂ and low pH inhibit a TASK-like potassium conductance, reducing potassium current. This leads to depolarisation of the cell membrane which leads to Ca²⁺ entry, excitation of glomus cells and consequent neurotransmitter release ^[6].

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 I (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, adenosine, ATP, 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 potentially.

Relay

The feedback from the carotid body is sent to the cardiorespiratory centers in the medulla oblongata via the afferent branches of the Glossopharyngeal nerve. The afferent fibres of the aortic body chemoreceptors are relayed by the Vagus nerve. These centers, in turn, regulate breathing and blood pressure.

Disorders

Micrograph of a carotid body tumor.

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

References

See also

• Aortic body
• Peripheral chemoreceptors

External links

• Respiratory physiology notes at Kirksville College of Osteopathic Medicine
• Carotid+body at eMedicine Dictionary

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