The ventilatory response to hypoxia is complex. First contact with hypoxia causes an increase in ventilation within seconds that reaches full intensity within minutes because of an increase in carotid sinus nerve (CSN) input to the brain stem. With continued exposure, ventilation increases further over days (ventilatory acclimatization). Initially, it was hypothesized that ventilatory acclimatization arose from a central nervous system (CNS) mechanism. Compensation for alkalosis in the brain and restoration of pH in the vicinity of central chemoreceptors was believed to cause the secondary increase in ventilation. However, when this hypothesis could not be substantiated, attention was turned to the peripheral chemoreceptors. With the lowering of arterial PO2 at high altitude, there is an immediate increase in firing of afferents from chemoreceptors in the carotid body. After peaking over the next few minutes, the firing rate of afferents begins to rise again within hours until a steady state is reached. This secondary increase occurs along with increase in neurotransmitter synthesis and release and altered gene expression followed by hypertrophy of carotid body glomus cells. Further exposure to hypoxia eventually leads to blunting of the CSN output and ventilatory response in some species. This mini review is about the altered structure and function of the carotid body at high altitude and the associated blunting of the chemoreceptor and ventilatory responses observed in some species.

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