Abstract
1. Cardiorespiratory response to acidosis is initiated by the carotid body. 2. The direct effect of extracellular pH (pHo) on the chloride currents of isolated chemoreceptor cells of the rat carotid body was investigated using the whole-cell patch-clamp technique. 3. On applying intra- and extracellular solutions with a symmetrical high-Cl- content and with the monovalent cations replaced with membrane-impermeant ones, an inwardly rectifying Cl- current was found. 4. The current activated slowly and did not display any time-dependent inactivation. Current activation was present at membrane potentials negative to 0 mV (pHo = 7.0). 5. The current was activated by extracellular acidosis and inhibited by alkalosis in the physiologically relevant pH range of 7.0-7.8. 6. The current was reduced by 0.1 mm Cd2+ to the level of the leak current and by 1 mM anthracene-9-carboxylic acid (9-AC) to about 40%, while 0.1 mM Ba2+ had no effect. 7. Application of 1 mM 9-AC caused a slow but statistically significant increase in the resting pHi (from a mean of 7.29 to 7.37 in 5 min) in clusters of chemoreceptor cells in CO2/HCO3--buffered media as measured with carboxy-SNARF-1. 8. When membrane potential changes were estimated in the cell-attached mode, 1 mM 9-AC hyperpolarized three out of five tested cells (by 14 mV in average) incubated in CO2/HCO3--buffered media. 9. In summary, chemoreceptor cells express an inwardly rectifying Cl- current, which is directly regulated by pHo. The current may participate in intracellular acidification and membrane depolarization during acidic challenge.