Abstract
Arterial chemoreceptors include the carotid and aortic bodies, which are small organs with a very high blood flow. Glomus cells in arterial chemoreceptors sense changes in arterial PO2, as well as PCO2 and pH by mechanisms involving ion channels and heme-containing molecules. Decreased PO2 and pH, and increased PCO2, depolarize glomus cells and trigger the release of neurotransmitters. An unidentified neurotransmitter depolarizes sensory nerve endings in arterial chemoreceptors so the intensity of the arterial stimulus is coded as the frequency of action potentials in the afferent nerves going to respiratory and cardiovascular centers in the medulla. Hypoxia and hypercapnia potentiate the effect of each other on the carotid body and the effect of PCO2 is mediated by changes in intracellular pH. The arterial chemoreceptor response to changes in arterial blood gases is extremely rapid (seconds) but they also exhibit plasticity and increased O2-sensitivity during chronic (hours-weeks) hypoxia.
Published Version
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