Abstract
We investigated the roles of IA and IDR potassium channels in action potential generation of avian intrapulmonary chemoreceptors (IPC). IPC are CO2‐sensing vagal afferents in avian lungs, with fast and inverse response to airway CO2 partial pressure (PCO2). Discharge frequency of a single cell IPC was recorded in 11 anesthesized, ventilated ducks. FICO2 was electronically controlled. Intravenous injection of voltage‐gated potassium‐channel blockers 4‐aminopyridine (4AP) or tetraethylammonium (TEA) disrupted the response to CO2. 4AP blocks the transient K current (IA), and TEA blocks the delayed rectifier current (IDR). A dose of 7 mg/kg of 4AP eliminated both phasic and tonic IPC sensitivities to FICO2, resulting in constant high‐frequency AP firing (p < 0.05). Low dosages of TEA had no effect on that sensitivity, although at high TEA doses (>; 20 mg/kg) the phasic (p < 0.05) but not tonic response to a step change in FICO2 disappeared. Our results suggest that transient voltage gated K channels (affected at low dosages of 4AP and high dosages of TEA) are involved in setting resting membrane potential in IPC. If IA in IPC is increased by CO2/H+ as it is in slowly adapting mammalian pulmonary stretch receptors, IA channel modulation by CO2/H+ may also underlie CO2 signal transduction in avian IPC. Support: NIH 2R15HL087269
Published Version
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