Hypoxic suppression of K+ currents in type I carotid body cells: selective effect on the Ca2(+)-activated K+ current.
Whole-cell K+ currents were recorded in isolated type I carotid body cells using the patch-clamp technique. Hypoxia (pO2 25 torr) reversibly suppressed K+ currents in a voltage-dependent manner: maximal effects were seen at low, positive test potentials, where the Ca2(+)-activated component of K+ currents was greatest. Enhancing this component with 5 microM BAY K 8644 exaggerated the effects of hypoxia, and when the component was inhibited (100 microM Cd2+ or 5 microM nifedipine) hypoxic effects were abolished. As hypoxia does not affect Ca2+ currents directly, these data indicate the suppressive effect of hypoxia is selective for the Ca2(+)-activated component of K+ currents in type I cells.
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University Laboratory of Physiology, Oxford, U.K.
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000818:Animals; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002344:Carotid Body / Q000166:cytology / Q000503:physiopathology*; D004095:Dihydropyridines / Q000378:metabolism; D004594:Electrophysiology; D000860:Hypoxia / Q000503:physiopathology*; D009543:Nifedipine / Q000494:pharmacology; D011188:Potassium / Q000502:physiology*; D051381:Rats
D002121:Calcium Channel Blockers; D004095:Dihydropyridines; D002104:Cadmium; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; C038806:1,4-dihydropyridine; D009543:Nifedipine; D011188:Potassium; D002118:Calcium