Two potassium‐channel blockers differently affect afferent signal of avian intrapulmonary chemoreceptors

We investigated the roles of I A and I DR potassium channels in action potential generation of avian intrapulmonary chemoreceptors (IPC). IPC are CO 2 ‐sensing vagal afferents in avian lungs, with fast and inverse response to airway CO 2 partial pressure (PCO 2 ). Discharge frequency of a single cell IPC was recorded in 11 anesthesized, ventilated ducks. FICO 2 was electronically controlled. Intravenous injection of voltage‐gated potassium‐channel blockers 4‐aminopyridine (4AP) or tetraethylammonium (TEA) disrupted the response to CO 2 . 4AP blocks the transient K current (I A ), and TEA blocks the delayed rectifier current (I DR ). A dose of 7 mg/kg of 4AP eliminated both phasic and tonic IPC sensitivities to FICO 2 , 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 FICO 2 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 I A in IPC is increased by CO 2 /H + as it is in slowly adapting mammalian pulmonary stretch receptors, I A channel modulation by CO 2 /H + may also underlie CO 2 signal transduction in avian IPC. Support: NIH 2R15HL087269