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 Ba 2+, a non-specific inhibitor of K + currents. In vitro changes in cytosolic calcium ([Ca 2+] c) and chemosensory...

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Bibliographic Details
Published in:Brain research 2001-04, Vol.897 (1), p.1-8
Main Authors: Rozanov, Charmaine, Roy, Arijit, Mokashi, Anil, Daudu, Peter, Lahiri, Sukhamay
Format: Article
Language:English
Subjects:
Animals
Barium - pharmacology
Biological and medical sciences
Cadmium - pharmacology
Calcium Channels - physiology
Cardiorespiratory control. Arterial mecano- and chemoreceptor
Carotid Body - drug effects
Carotid Body - physiology
Chelating Agents - pharmacology
Egtazic Acid - pharmacology
Electron Transport - physiology
Fundamental and applied biological sciences. Psychology
Ganglionic Blockers - pharmacology
Hexamethonium - pharmacology
Hypoxia
Hypoxia - physiopathology
Mitochondria - physiology
Mitochondrial respiratory chain
Oligomycins - pharmacology
Post synaptic carotid sinus nerve
Potassium Channels - physiology
Rats
Receptor-mediated Ca 2+ entry
Stimulation, Chemical
Uncoupling Agents - pharmacology
Vertebrates: respiratory system
Voltage-gated Ca 2+ channel
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Summary: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 Ba 2+, a non-specific inhibitor of K + currents. In vitro changes in cytosolic calcium ([Ca 2+] c) and chemosensory discharge were studied to measure the effect of Ba 2+. In normal Tyrode buffer, Ba 2+ (3 and 5 mM) significantly increased carotid sinus nerve (CSN) discharge over baseline firing rates under normoxia (P o 2∼120 Torr) from ∼150 to ∼600 imp/0.5 s. However, addition of 200 μM Cd 2+ which completely blocked increase in CSN activity stimulated by hypoxia (P o 2∼30 Torr), hypercapnia (P co 2∼60 Torr, P o 2∼120 Torr) and high CO (P co∼550 Torr, P o 2∼120 Torr) did not significantly inhibit Ba 2+-stimulated CSN discharge. The response to hypoxia is abolished with Ca 2+-free tyrode buffer containing 10 mM EGTA. Yet, in the same buffer, Ba 2+ increased CSN discharge from ∼2 to ∼180 imp/0.5 s. With 200 μM Cd 2+ and 10 mM EGTA, Ba 2+ still increased CSN discharge from ∼2 to ∼150 imp/0.5 s. Oligomycin (2 μg) abolished the hypoxic response. However, in the presence of oligomycin CSN response to Ba 2+ was significant. Since Ba 2+ increased neural discharge under conditions where hypoxia stimulated CSN discharge is completely abolished, we suggest that the effect of Ba 2+ on CSN discharge may not have anything to do with the oxygen sensing mechanism in the CB.
ISSN:0006-8993
1872-6240
DOI:10.1016/S0006-8993(00)03310-2