Abstract
Exposure of humans and animals to chronic hypoxia causes hypertrophy of the chemosensory carotid body (McGregor et al., 1988), and sensitization of the ventilatory reflex (Barnard et al., 1987; Nielsen et al., 1987). The underlying mechanisms are unclear but are likely to involve the glomus or type 1 cells, which are now generally considered to be the oxygen sensors (Gonzalez et al., 1992). These structural and functional changes may be triggered by the direct, chronic stimulation of glomus cells by low PO2, perhaps acting via the intracellular second messenger cAMP (see Wang et al. 1991). To address this we investigated whether chronic exposure of carotid body cultures to hypoxia (6% O2) or cAMP analogs leads to modification in glomus cells properties that may explain carotid body plasticity during ventilatory acclimatization.
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