tetrodotoxin and Acidosis--Respiratory

Substitution of extracellular Na+ with N-methyl D-glucamine caused marked hyperpolarisation in rat isolated carotid body type I cells, suggesting the presence of a standing Na+ conductance. Choline substitution produced smaller hyperpolarisations, whilst Li+ was virtually without effect. This Na+ conductance was not blocked by amiloride, tetrodotoxin, Zn2+ or Gd3+ and did not arise from electrogenic Na-glucose co-transport, since substitution of glucose with sucrose could not mimic the effects of Na+ substitution. Hypoxia and acidosis did not modify the tonic Na+ influx. Our results suggest that Na+ influx provides a constant depolarising influence on type I cells which acts to shift membrane potential beyond that required for initiation of neurosecretion, an essential step in carotid body chemotransduction.

Topics: Acid-Base Equilibrium; Acidosis, Respiratory; Amiloride; Animals; Carotid Body; Cells, Cultured; Choline; Gadolinium; Homeostasis; Hydrogen-Ion Concentration; Hypoxia; Lithium; Meglumine; Membrane Potentials; Oxygen; Patch-Clamp Techniques; Potassium Channels; Rats; Signal Transduction; Sodium; Sodium Channels; Tetrodotoxin; Zinc