Abstract

IPC are respiratory chemoreceptors that exhibit SFA, have phasic and tonic CO2 sensitivity, and help control breathing in birds. In IPC, large changes in PCO2, pHi, and [HCO3]i occur with each breath. Here we test the hypothesis that Cl‐ transmembrane flux may be involved in IPC CO2 transduction to balance intracellular [HCO3‐] changes. Furosemide (FU), an equipotent inhibitor of both K+ ‐Cl‐ cotransport (KCC), which allows for Cl‐ efflux driven by the K+ gradient, and Na+ ‐K+ ‐2Cl‐ cotransport (NKCC), which allows for Cl‐ influx driven by the Na+ gradient, was given to anesthetized Anas platyrhynchos (N=6) while recording single‐unit IPC. FU progressively reduced SFA at 10‐40 mg/kg (p蠄0.0001). In contrast, tonic IPC discharge was decreased at low FU doses (0.5‐5 mg/kg, p蠄0.0001) but increased at higher dosages (10‐40 mg/kg, p蠄0.0001). Results suggest that IPC SFA and tonic CO2 sensitivity are influenced by KCC and/or NKCC, presumably by reducing ability of the cell to produce Cl‐ counter movements required by phasic [HCO3‐] changes.Grant Funding Source: Supported by NIH R15 HL087269‐02

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