Barium-stimulated chemosensory activity may not reflect inhibition of background voltage-insensitive K+ channels in the rat carotid body

To test the hypothesis that the voltage-insensitive background leak K+ chan nel is responsible for the oxygen-sensitive properties of glomus cells in t he rat carotid body (CB) we used Ba2+, a non-specific inhibitor of K+ curre nts. In vitro changes in cytosolic calcium ([Ca2+](c)) and chemosensory dis charge were studied to measure the effect of Ba2+. In normal Tyrode buffer, Ba2+ (3 and 5 mM) significantly increased carotid sinus nerve (CSN) discha rge over baseline firing rates under normoxia (Po(2)similar to 120 Torr) fr om similar to 150 to similar to 600 imp/0.5 s. However, addition of 200 muM Cd2+ which completely blocked increase in CSN activity stimulated by hypox ia (Po(2)similar to 30 Torr), hypercapnia (Pco(2)similar to 60 Torr, Po(2)s imilar to 120 Torr) and high CO (Pco similar to 550 Torr, Po(2)similar to 1 20 Torr) did not significantly inhibit Ba2+-stimulated CSN discharge. The r esponse to hypoxia is abolished with Ca2+-free tyrode buffer containing 10 mM EGTA. Yet, in the same buffer, Ba2+ increased CSN discharge from similar to2 to similar to 180 imp/0.5 s. With 200 muM Cd2+ and 10 mM EGTA, Ba2+ st ill increased CSN discharge from similar to2 to similar to 150 imp/0.5 s. O ligomycin (2 mug) abolished the hypoxic response. However, in the presence of oligomycin CSN response to Ba2+ was significant. Since Ba2+ increased ne ural discharge under conditions where hypoxia stimulated CSN discharge is c ompletely abolished, we suggest that the effect of Ba2+ on CSN discharge ma y not have anything to do with the oxygen sensing mechanism in the CB. (C) 2001 Elsevier Science B.V. All rights reserved.