Genetic Disorders. Central Chemoreceptors. Overview The Central Chemoreceptors are an anatomical collection of neuronal chemoreceptors located just beneath the ventral surface of the brainstem's medulla, a few hundred microns away from the brainstem respiratory centers.
The central chemoreceptors are critical sensors of arterial carbon dioxide and are the key sensory component of a negative feedback loop which controls respiratory activity in an attempt to maintain relatively constant levels of arterial carbon dioxide as described in integrated respiratory control. Sensory Mechanism Experimental studies have demonstrated that the central chemoreceptors are most directly sensitive to changes in their surrounding extracellular fluid pH, which given their anatomical location would mean the CSF.
However, the blood brain barrier is relatively impermeable to hydrogen and bicarbonate ions; consequently, the central chemoreceptors cannot respond quickly to changes in the blood pH. Although blood pH is not closely linked to the CSF pH, the partial pressure of arterial carbon dioxide displays a tight relationship with the CSF pH through a notable mechanism.
It is presumed that this situation also applies to humans even though direct experimental confirmation is probably not possible. The final level of ventilation is dependent on the balance between the stimulation from the metabolic acidosis and the inhibition from the fall in pCO 2 but the pH is not returned completely to its previous value. The peripheral chemoreceptors are the aortic and carotid bodies. They are anatomically separate from the carotid sinus baroreceptors and should not be confused with them.
The peripheral chemoreceptors respond to changes in pO 2 , pCO 2 and pH. The peripheral chemoreceptors may be more important than this would indicate as they can respond more rapidly to relatively acute alterations in pCO 2.
The carotid bodies also respond directly to a decrease in arterial pH even if pO 2 and pCO 2 are held constant. The peripheral chemoreceptors and the central chemoreceptors both contribute to causing the hyperventilation Kussmaul respirations that accompany metabolic acidosis. This increase in ventilation will lower arterial pCO 2 and this will be sensed by the central and peripheral chemoreceptors and ventilation will be inhibited.
This will progressively remove the mostly central chemoreceptor mediated inhibition of ventilation. Any situation with hypoxia too low oxygen levels will cause a feedback response that increases ventilation to increase oxygen intake.
Vomiting causes alkalosis and diarrhea causes acidosis, which will cause an appropriate respiratory feedback response. Key Terms hypoxia : A system-wide deficiency in the levels of oxygen that reach the tissues. Chemoreceptors A chemoreceptor, also known as chemosensor, is a sensory receptor that transduces a chemical signal into an action potential.
The main chemoreceptors involved in respiratory feedback are: Central chemoreceptors: These are located on the ventrolateral surface of medulla oblongata and detect changes in the pH of spinal fluid.
They can be desensitized over time from chronic hypoxia oxygen deficiency and increased carbon dioxide. Peripheral chemoreceptors: These include the aortic body, which detects changes in blood oxygen and carbon dioxide, but not pH, and the carotid body which detects all three.
They do not desensitize, and have less of an impact on the respiratory rate compared to the central chemoreceptors. Chemoreceptors detect the levels of carbon dioxide in the blood by monitoring the concentrations of hydrogen ions in the blood.
Chemoreceptor regulation of breathing is a form of negative feedback. The goal of this system is to keep the pH of the blood stream within normal neutral ranges, around 7. A chemoreceptor, also known as chemosensor, is a sensory receptor that transduces a chemical signal into an action potential.
The action potential is sent along nerve pathways to parts of the brain, which are the integrating centers for this type of feedback. There are many types of chemoreceptors in the body, but only a few of them are involved in respiration. The respiratory chemoreceptors work by sensing the pH of their environment through the concentration of hydrogen ions.
Because most carbon dioxide is converted to carbonic acid and bicarbonate in the bloodstream, chemoreceptors are able to use blood pH as a way to measure the carbon dioxide levels of the bloodstream.
Negative feedback responses have three main components: the sensor, the integrating sensor, and the effector. For the respiratory rate, the chemoreceptors are the sensors for blood pH, the medulla and pons form the integrating center, and the respiratory muscles are the effector.
Consider a case in which a person is hyperventilating from an anxiety attack. Their increased ventilation rate will remove too much carbon dioxide from their body. Without that carbon dioxide, there will be less carbonic acid in blood, so the concentration of hydrogen ions decreases and the pH of the blood rises, causing alkalosis.
In response, the chemoreceptors detect this change, and send a signal to the medulla, which signals the respiratory muscles to decrease the ventilation rate so carbon dioxide levels and pH can return to normal levels. There are several other examples in which chemoreceptor feedback applies. A person with severe diarrhea loses a lot of bicarbonate in the intestinal tract, which decreases bicarbonate levels in the plasma. As bicarbonate levels decrease while hydrogen ion concentrations stays the same, blood pH will decrease as bicarbonate is a buffer and become more acidic.
In cases of acidosis, feedback will increase ventilation to remove more carbon dioxide to reduce the hydrogen ion concentration.
Conversely, vomiting removes hydrogen ions from the body as the stomach contents are acidic , which will cause decreased ventilation to correct alkalosis.
Chemoreceptor feedback also adjusts for oxygen levels to prevent hypoxia, though only the peripheral chemoreceptors sense oxygen levels. In cases where oxygen intake is too low, feedback increases ventilation to increase oxygen intake.
A more detailed example would be that if a person breathes through a long tube such as a snorkeling mask and has increased amounts of dead space, feedback will increase ventilation. Respiratory feedback : The chemoreceptors are the sensors for blood pH, the medulla and pons form the integrating center, and the respiratory muscles are the effector. Evaluate the effect of proprioception the sense of the relative position of the body and effort being employed in movement on breathing.
The lungs are a highly elastic organ capable of expanding to a much larger volume during inflation. While the volume of the lungs is proportional to the pressure of the pleural cavity as it expands and contracts during breathing, there is a risk of over-inflation of the lungs if inspiration becomes too deep for too long.
Physiological mechanisms exist to prevent over-inflation of the lungs. Cardiac and respiratory branches of the vagus nerve : The vagus nerve is the neural pathway for stretch receptor regulation of breathing. The Hering—Breuer reflex also called the inflation reflex is triggered to prevent over-inflation of the lungs. There are many stretch receptors in the lungs, particularly within the pleura and the smooth muscles of the bronchi and bronchioles, that activate when the lungs have inflated to their ideal maximum point.
These stretch receptors are mechanoreceptors, which are a type of sensory receptor that specifically detects mechanical pressure, distortion, and stretch, and are found in many parts of the human body, especially the lungs, stomach, and skin. They do not detect fine-touch information like most sensory receptors in the human body, but they do create a feeling of tension or fullness when activated, especially in the lungs or stomach. When the lungs are inflated to their maximum volume during inspiration, the pulmonary stretch receptors send an action potential signal to the medulla and pons in the brain through the vagus nerve.
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