These act to detect the changes in pH of nearby cerebrospinal fluid (CSF) that are indicative of altered oxygen or carbon dioxide concentrations available to brain tissues.
An increase in carbon dioxide causes tension of the arteries, often resulting from increased CO2 output (hypercapnia), indirectly causes the blood to become more acidic; the cerebrospinal fluid pH is closely comparable to plasma, as carbon dioxide easily diffuses across the blood–brain barrier.
The central chemoreception system has also been shown experimentally to respond to hypercapnic hypoxia (elevated CO2, decreased O2) and aqueous sodium cyanide injection into the whole animal[2] and in vitro slice preparation.
These methods can be used to mimic some forms of hypoxic hypoxia and they are currently being studied including the detection of variation in arterial CO2 tension acting as a quick-response-system for short term (or emergency) regulation.
Respiratory arrest and circulatory shock (these conditions decrease arterial pO2 and pH, and increase arterial pCO2) dramatically increase chemoreceptor activity leading to enhanced sympathetic outflow to the heart and vasculature via activation of the vasomotor center in the medulla.