Abstract
O2 and CO2/pH are detected by the carotid bodies (CBs) and central respiratory chemoreceptors, respectively. CB activity appears to modulate central chemoreceptor activity, suggesting chemoreceptor interdependence. Here, we studied the effects of CB denervation in CO2‐insensitive Brown Norway (BN) and CO2‐sensitive Dahl Salt‐sensitive (SS) and Sprague Dawley (SD) rats by chronic measurements of ventilation (VE) and blood gases at rest, and during hypercapnia (7% CO2) or hypoxia (12% O2) before and for 21 days (d) after CBD. Peak eupneic hypoventilation (Δ PaCO2) occurred 1–2 d post‐CBD in all strains, increasing 11.0 (SS), 9.4 (BN) and 7.0 (SD) mmHg. Resting PaCO2 returned to control by 12 d post‐CBD (BN and SD), but remained elevated (+3.9 mmHg) in SS rats. SS and SD rats showed high sensitivity (VE ~300% of control) and BN rats a low sensitivity (VE ~150% of control) to hypercapnia pre‐CBD, which was unaffected by CBD. In addition, CO2 sensitivity (measured as ΔVE/ΔPaCO2) was also unaffected by CBD in all strains, despite a near‐complete loss of the hypoxic ventilatory response and attenuation of the ventilatory response to i.v. NaCN. As seen in other species, these data suggest that CBD in rats leads to eupneic hypoventilation and elimination of the hypoxic ventilatory response, but the lack of effect on CO2 sensitivity does not support the concept of chemoreceptor interdependence. Supported by NIH HL097033.
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