It is a peripheral receptor located in the carotid body (mainly responsible for respiration) and the aortic body (mainly responsible for blood pressure).

When arterial PO2 decreases and PCO2 or H concentration increases, peripheral chemoreceptors are stimulated, and the impulses are transmitted to the nucleus of the solitary tract along the sinus nerve and vagus nerve respectively, which reflexively causes accelerated breathing and changes in blood circulation function.

The physiological stimulation of central chemoreceptors is H in cerebrospinal fluid and local extracellular fluid.

However, CO2 can quickly pass through the blood-brain barrier, increasing the H concentration in the extracellular fluid around the chemoreceptors, thereby stimulating the central chemoreceptors, causing excitement in the respiratory center, deepening and accelerating breathing, and increasing lung ventilation.

Central chemoreceptors adapt to rising CO2 concentrations

CO2 is known to be the most important physiological chemical factor in regulating respiratory movements.

A certain level of PCO2 is necessary to maintain the basic activity of the respiratory center. Hyperventilation can also inhibit respiratory movement due to increased CO2 discharge. An increase in blood PCO2 to a certain extent can enhance respiratory movement, but if it exceeds a certain limit, it will inhibit it.

How CO2 stimulates breathing

Central chemoreceptors respond slowly, so when arterial blood PCO2 suddenly increases, peripheral chemoreceptors play an important role in causing a rapid respiratory response. In addition, when the sensitivity of central chemoreceptors to CO2 is reduced or adapted, the role of peripheral chemoreceptors becomes particularly important.

H in the blood mainly works by stimulating peripheral chemoreceptors, while H in the cerebrospinal fluid is the most effective stimulator of central chemoreceptors.

Central chemoreceptors are more sensitive to H than peripheral chemoreceptors, but H passes through the blood-brain barrier more slowly, limiting its effect on central chemoreceptors.

The stimulating effect of low O2 on respiratory movement is entirely achieved through peripheral chemoreceptors.

The direct effect of low O2 on the central nervous system is inhibition. The excitatory effect of low O2 on the respiratory center through peripheral chemoreceptors can counter its direct inhibitory effect on the center. However, in severe O2 deficiency, if the reflex effect of peripheral chemoreceptors is not enough to overcome the direct inhibitory effect of low O2 on the central nervous system, respiratory movement will be weakened.