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+ channel is responsible for the oxygen-sensitive properties of glomus cells in the rat carotid body (CB) we used Ba2+, a non-specific inhibitor of K+ currents. In vitro changes in cytosolic calcium ([Ca2+]c) and chemosensory discharge were studied to measure the effect of Ba2+. In normal Tyrode buffer, Ba2+ (3 and 5 mM) significantly increased carotid sinus nerve (CSN) discharge over baseline firing rates under normoxia (PO2 approximately 120 Torr) from approximately 150 to approximately 600 imp/0.5 s. However, addition of 200 microM Cd2+ which completely blocked increase in CSN activity stimulated by hypoxia (PO2 approximately 30 Torr), hypercapnia (PCO2 approximately 60 Torr, PO2 approximately 120 Torr) and high CO (PCO approximately 550 Torr, PO2 approximately 120 Torr) did not significantly inhibit Ba2+-stimulated CSN discharge. The response to hypoxia is abolished with Ca2+-free tyrode buffer containing 10 mM EGTA. Yet, in the same buffer, Ba2+ increased CSN discharge from approximately 2 to approximately 180 imp/0.5 s. With 200 microM Cd2+ and 10 mM EGTA, Ba2+ still increased CSN discharge from approximately 2 to approximately 150 imp/0.5 s. Oligomycin (2 microg) abolished the hypoxic response. However, in the presence of oligomycin CSN response to Ba2+ was significant. Since Ba2+ increased neural discharge under conditions where hypoxia stimulated CSN discharge is completely abolished, we suggest that the effect of Ba2+ on CSN discharge may not have anything to do with the oxygen sensing mechanism in the CB.
Rozanov
C
C
Department of Physiology, University of Pennsylvania School of Medicine, B400 Richards Building, 3700 Hamilton Walk, Philadelphia, PA 19104-6085, USA.
Roy
A
A
Mokashi
A
A
Daudu
P
P
Lahiri
S
S
D000818:Animals; D001464:Barium / Q000494:pharmacology*; D002104:Cadmium / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology; D002344:Carotid Body / Q000187:drug effects* / Q000502:physiology*; D002614:Chelating Agents / Q000494:pharmacology; D004533:Egtazic Acid / Q000494:pharmacology; D004579:Electron Transport / Q000502:physiology; D005730:Ganglionic Blockers / Q000494:pharmacology; D018738:Hexamethonium / Q000494:pharmacology; D000860:Hypoxia / Q000503:physiopathology; D008928:Mitochondria / Q000502:physiology; D009840:Oligomycins / Q000494:pharmacology; D015221:Potassium Channels / Q000502:physiology*; D051381:Rats; D013268:Stimulation, Chemical; D014475:Uncoupling Agents / Q000494:pharmacology
D015220:Calcium Channels; D002614:Chelating Agents; D005730:Ganglionic Blockers; D009840:Oligomycins; D015221:Potassium Channels; D014475:Uncoupling Agents; D002104:Cadmium; D001464:Barium; D018738:Hexamethonium; D004533:Egtazic Acid