Calcium channels of cultured rat glomus cells in normoxia and acute hypoxia.
Glomus cells harvested from Wistar rat carotid bodies were cultured for 4 to 7 days. Inward calcium currents elicited by voltage ramps (0.24 V/s) or pulses were recorded during voltage-clamping in the whole-cell and perforated patch configurations. Currents were enhanced by an excess of [Ca(2+)](o), barium and BayK 8644, and depressed or eliminated by cobalt or nifedipine. Single calcium channels were studied by patch-clamping in the cell-attached configuration with voltage clamp pulses ranging from 0.5 to 50 s. Channel conductances (g) decreased and open times (OT) increased as clamp pulses increased in duration. For comparisons, conductances and OTs obtained with short (0.5-1 s) and long (6-12 s) pulses were grouped as SVH and LVH, respectively. SVH conductances were higher and OTs shorter when compared to LVH. BayK 8644 increased conductances and OT during SVH but this agonist decreased g during LVH. Nifedipine either eliminated channel activity, had no effects or depressed g and OT. Hypoxia (pO(2) 30 Torr) induced by 100% N(2) significantly increased calcium currents in normal bathing solutions and during exposure to 110 mM BaCl(2) in whole-cell and perforated patch recordings. Sodium dithionite (Na(2)S(2)O(4)), lowering pO(2) to 10 Torr, also increased the amplitude of calcium currents, but shifted to more positive voltages the onset and trough (maximum) of calcium currents. N(2)-induced hypoxia increased g and reduced OT during SVH but had opposite effects with longer pulses: conductance decreased and open times increased. N(2)-induced hypoxia increased the numbers of active channels (from 1 to 35) over a mean normoxic level of 47 per cell. It is suggested that increased calcium currents accompany calcium inflow in glomus cells, but calcium influx may not depend exclusively on this mechanism.
Jiang
R G
RG
Department of Physiology, University of Utah School of Medicine, Research Park, Salt Lake City, UT 84108-1297, USA.
Eyzaguirre
C
C
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000208:Acute Disease; D000818:Animals; D001464:Barium / Q000494:pharmacology; D002118:Calcium / Q000493:pharmacokinetics; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology*; D002344:Carotid Body / Q000166:cytology* / Q000502:physiology*; D002478:Cells, Cultured; D003035:Cobalt / Q000494:pharmacology; D000860:Hypoxia / Q000503:physiopathology*; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009543:Nifedipine / Q000494:pharmacology; D009584:Nitrogen / Q000494:pharmacology; D010100:Oxygen / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D051381:Rats; D017208:Rats, Wistar
D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D001464:Barium; D003035:Cobalt; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D009543:Nifedipine; D009584:Nitrogen; D010100:Oxygen; D002118:Calcium