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1 Department of Biological Sciences, Northern Arizona University, Flagstaff, Arizona 86011-5640; 2 Division of Neurobiology, Physiology and Behavior, University of California, Davis, California 95616; and 3 Department of Physiology and Biophysics, State University of New York, Stony Brook, New York 11794-8661
Avian intrapulmonary chemoreceptors (IPC) are vagal respiratory afferents that are inhibited by high lung PCO2 and excited by low lung PCO2. Previous work suggests that increased CO2 inhibits IPC by acidifying intracellular pH (pHi) and that pHi is determined by a kinetic balance between the rate of intracellular carbonic anhydrase-catalyzed CO2 hydration/dehydration and transmembrane extrusion of acids and/or bases by various exchangers. Here, the role of amiloride-sensitive Na+/H+ exchange (NHE) in the IPC CO2 response was tested by recording single-unit action potentials from IPC in anesthetized ducks, Anas platyrhynchos. For each of the IPC tested, blockade of the NHE using dimethyl amiloride (DMA) elicited a marked (>50%) dose-dependent decrease in mean IPC discharge (P < 0.05), suggesting that NHE is important for pHi regulation and CO2 transduction in IPC. In addition, activation of the NHE using 12-O-tetradecanoylphorbol 13-acetate stimulated six of the seven IPC tested, although the overall effect was not statistically significantly (P = 0.07). Taken together, these findings suggest that CO2 transduction in IPC is dependent on transmembrane NHE although it is likely to be much slower than carbonic anhydrase-catalyzed hydration-dehydration of CO2.
carbon dioxide chemosensitivity; intracellular pH regulation; respiratory control; neuron; acid; base
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