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The carotid body monitors the blood's pH, pCO2, and pO2
When the carotid body senses acidemia, hypercapnea, or hypoxia, autonomic firing to the brain is sent via the Glossopharyngeal nerve.
The carotid body sends these signals via the glossopharyngeal nerve to the DRG.
This imput causes hyperventilation and leads to a respiratory alkalosis that limits the rise in ventilation and leads to symptoms of AMS.
Then acetazolamide interferes with the central chemorecepters in the medulla.
The central chemoreceptors also recieve the imput and constantly initiate negative feedback loops which act to control our respiratory system. An increase in pCO2 leads to an increase in ventilation
Carbonic anhydrase in the central chemoreceptor aids in the conversion of excess carbon dioxide to carbonic acid and bicarbonate ions
Acetazolamide blocks the CA and diminishes the rise of bicarbonate ions. This leads to metabolic acidosis produced by renal bicarbonate diuresis.
The metabolic acidosis increases output of signals from the central chemoreceptors.
Increased CCR output attenuates the effects of respiratory alkalosis by increasing PaO2.
The renal acidosis is caused by the CA inhibitory effects of acetazolamide.
In the kidneys, CA inhibition also leads to metabolic acidosis which increases CCR output.
By inhibiting CA, acetazolamide increases metabolic acidosis and counteracts the effects of respiratory alkalosis due to increased output of chemoreceptors in the medulla.