Avian intrapulmonary chemoreceptors (IPC) are vagal sensory neurons that participate in the control of breathing. IPC action potential frequency is inversely proportional to PCO₂, but it is unclear whether low PCO₂ or high pH is the immediate stimulus for signal transduction in IPC. To address this question, comparisons were made between single cell neural responses of 34 IPC recorded in 6 anesthetized ducks (Anas platyrhynchos) acclimatized 12 days to 7.5% inspired CO₂ and 22 IPC recorded in 9 normal anesthetized ducks. We hypothesized that if respiratory-linked pH changes determine IPC activity, action potential frequency as a function of inspiratory PCO₂ (PI_CO2) should be greater after acclimatization due to metabolic acid-base compensation and higher pH. Conversely, if PCO₂ alone determines IPC discharge, action potential frequency vs. PCO₂ should be unchanged by acclimatization. Results indicate that after acclimatization ventilation was depressed at 28 and 42 Torr PI_CO2 (P < 0.05) and mean plasma pH at 40 Torr PCO₂ increased from 7.38 ± 0.03 to 7.56 ± 0.02 (P < 0.05), indicating significant metabolic acid-base compensation and HCO₃ retention. Mean IPC discharge rate was elevated by CO₂ acclimatization at all PCO₂ studied. In acclimatized vs. normal animals, regression analysis of IPC discharge as a function of lnPCO₂ showed increased mean intercepts of 81.1 ± 4.0 vs. 48.4 ± 3.6 impulses/s (P < 0.05) and increased mean slopes of 19.0 ± 1.0 vs. 12.0 ± 1.1 impulses · s¹ · lnPCO₂¹ (P < 0.05). Results indicate that IPC response to CO₂ is mediated by H⁺ from CO₂ hydration and not by CO₂ directly.

intracellular pH; CO₂ signal transduction; ventilatory control

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