Chemoreceptors are stimulated by a change in the chemical composition of their immediate environment. There are many types of chemoreceptor spread throughout the body which help to control different processes including taste, smell and breathing.
In this article, we shall focus on how our respiratory system is regulated by central and peripheral chemoreceptors. Both types of these chemoreceptors have slightly different mechanisms but work alongside each other to help our bodies control the pH, partial pressure of oxygen (pO2) and partial pressure of carbon dioxide (pCO2) within our blood.
Located in both the carotid body and the aortic body, these receptors detect large changes in pO2 as the arterial blood supply leaves the heart. These chemoreceptors are relatively insensitive but their effects are almost instantaneous.
If an abnormally low pO2 is detected, afferent impulses travel to the respiratory centres in the brainstem. A number of responses are then coordinated which aim to increase the pO2 again. These include:
- Increasing the respiratory rate and tidal volume, to allow more oxygen to enter the lungs and subsequently diffuse into the blood
- Directing blood flow towards the kidneys and the brain (as these organs are the most sensitive to hypoxia)
- Increasing Cardiac Output in order to maintain blood flow, and therefore oxygen supply to the body’s tissues.
Located in the medulla oblongata of the brainstem, these receptors are more sensitive and detect smaller changes in arterial pCO2. These chemoreceptors constantly initiate negative feedback loops which act to control our respiratory system:
- An increase in pCO2 leads to an increase in ventilation. This results in more CO2 being blown off and so the pCO2 returns to normal
- A decrease in pCO2 leads to a decrease in ventilation. This results in more CO2 being retained in our lungs and so the pCO2 returns to normal.
The mechanism behind how central chemoreceptors detect the arterial pCO2 is actually slightly more complicated than first thought. In fact, these receptors actually detect changes in the pH of the Cerebral Spinal Fluid (CSF).
The pH of the CSF is established by the ratio of pCO2 : [HCO3–].
The HCO3– levels remain relatively constant, whereas CO2 freely diffuses across the blood brain barrier (from the arterial blood supply into the CSF). This means, in the short term, the pH of the CSF is approximately inversely proportional to the arterial pCO2. As described above, a small drop in pCO2 leads to an increase in pH of the CSF and subsequently stimulates the respiratory centres to decrease ventilation and vice versa.
However if pCO2 levels stay abnormal over a substantial period of time, e.g. three days or more, specialised cells (called choroid plexus cells) within the blood brain barrier allow HCO3– ions to enter the CSF. As such the system can be ‘reset’ to a different pCO2 by manipulating the pH – which can be relevant in certain diseases, such as Chronic Obstructive Pulmonary Disease (COPD).
Clinical Relevance – Hypoventilation
Hypoventilation leads to a build-up of carbon dioxide within the body, commonly known as hypercapnia, which causes the blood to become acidic when dissolved. This is dangerous as it can cause vital proteins, such as enzymes, to denature.
Common causes include: COPD, chest wall deformities, neurological defects and obesity.
Clinical Relevance – Hyperventilation
Hyperventilation leads to a depletion of carbon dioxide within the body, known clinically as hypocapnia, which causes our blood to become more alkaline. This decreases free calcium levels and can lead to symptoms such as pins and needles (paraesthesia) or muscle cramps, due to the increased excitability of nerves and muscles
Common causes include: anxiety, heart failure and pulmonary Embolism.