Oxygen Sensing by Arterial Chemoreceptors

  • Ashima Anand
  • A. S. Paintal
Part of the Clinical Physiology Series book series (CLINPHY)


The physiology of arterial chemoreceptors, as well as other aspects relating to them, has been presented relatively recently in an authoritative review by Eyzaguirre et al. (11). This chapter reveals that from the very beginning, arterial chemoreceptors have been believed to detect the chemical composition of the blood, specifically the partial pressure of oxygen in the blood and also possibly the partial pressure of carbon dioxide. The oxygen content of the blood was ruled out as an important factor because Comroe and Schmidt (8) found that these chemoreceptors were apparently not stimulated when the oxygen content of the blood was reduced. From this finding, it followed that the dissolved oxygen in the plasma was enough for their metabolic needs (8). A few years later, Landgren and Neil (26) showed that the carotid chemoreceptors were also markedly stimulated after hemorrhage. Neil (32) advanced the view that stagnation led to the accumulation of some excitatory substance (metabolites) that constituted the excitatory substance of the chemoreceptors. The local concentration of the metabolite that constituted the stimulus for the chemoreceptors determined the degree of stimulation of these chemoreceptors. This concentration depended on the level of oxygen tension in the blood and the rate at which it was removed from the blood circulating through the sinusoids (32). Then came the classic paper by Daly et al. (9) showing that the oxygen consumption by the carotid body was not small, as assumed, but very large—even greater than that of the cerebral cortex—and that the blood flow through the carotid body was also large. This was consistent with its large rate of oxygen consumption. These two new findings should have resulted in the revision of the metabolite hypothesis; but, possibly, this was not done because just 2 years earlier Duke et al. (10) had shown that the chemoreceptors were not stimulated by reducing the oxygen content to as low as 25% of normal by administering carbon monoxide (CO), an observation that they felt was consistent with the earlier views of Comroe and Schmidt (8).


Carotid Body Excitatory Effect Sensory Receptor Sympathetic Outflow Peripheral Chemoreceptor 
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© American Physiological Society 1991

Authors and Affiliations

  • Ashima Anand
  • A. S. Paintal

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