Journal
JOURNAL OF PHYSIOLOGY-LONDON
Volume 525, Issue 1, Pages 135-142Publisher
WILEY
DOI: 10.1111/j.1469-7793.2000.00135.x
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1. The biophysical and pharmacological properties of an oxygen-sensitive background K+ current in rat carotid body type-I cells were investigated and compared with those of recently cloned two pore domain K+ channels. 2. Under symmetrical K+ conditions the,oxygen-sensitive whole cell K+ current had a linear dependence on voltage indicating a lack of intrinsic voltage sensitivity 3. Single channel recordings identified a K+ channel, open at resting membrane potentials, that was inhibited by hypoxia. This channel had a single channel conductance of 14 pS, flickery kinetics and showed little voltage sensitivity except at extreme positive potentials. 4. Oxygen-sensitive current was inhibited by 10 mM barium (57% inhibition), 200 mu M zinc (53% inhibition), 200 mu M bupivacaine (55% inhibition) and 1 mM quinidine (105% inhibition). 5. The general anaesthetic halothane (1.5%) increased the oxygen-sensitive K+ current (by 176%). Halothane (3 mM) also stimulated single channel activity in inside-out patches (by 240%). Chloroform had no effect un background K+ channel activity 6. Acidosis (pH 6.4) inhibited the oxygen-sensitive background K+ current (by 56%) and depolarised type-I cells. 7. The pharmacological and biophysical properties of the background K+ channel are, therefore, analogous to those of the cloned channel TASK-1. Using in situ hybridisation TASK-1 mRNA was found to be expressed in type-I cells. We conclude that the oxygen- and acid-sensitive background K+ channel of carotid body type-I cells is likely to be an endogenous TASK-1-like channel.
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