Intrapulmonary chemoreceptors (IPC) are exquisitely sensitive to steady and dynamically changing CO2 levels in avian lungs, but the mechanism of chemotransduction remains unknown. We sought a model that could explain the following experimental data: (1) hydratable acidic gases like CO2 and SO2 inhibit IPC discharge; (2) membrane permeant carbonic anhydrase (CA) inhibitors block CO2 response and produce near maximal IPC discharge rates (fIPC) at all CO2 levels; (3) chronic acclimatization to elevated CO2 increases fIPC (and body fluid pH) at any given PCO2; (4) chronic metabolic acidosis reduces fIPC (and body fluid pH) at most PCO2; (5) acute metabolic acidosis or alkalosis (which may not alter intracellular pHi) has little effect on fIPC. We propose the following model of IPC chemotransduction: When CO2 is low, IPC are excited by high pHi which may directly decrease a repolarizing membrane ton channel conductance (eg. for K+), or increase a depolarizing ion channel conductance (eg. for Na+). This excitation should rapidly decrease when pHi falls with elevated PCO2. We also propose a continuous active transport of H+ out of IPC endings with first order kinetics, which gives rise to adaptation with dynamically changing CO2 signals, and near maximal IPC discharge at all PCO2 levels when CA is inhibited (pHi always high). This model may be tested with ion channel blockers and active transport inhibitors.
|Original language||English (US)|
|State||Published - Dec 1 1997|
ASJC Scopus subject areas
- Molecular Biology