Effects of different ions on resting polarization and on the mass receptor potential of carotid body chemosensors.
The carotid body and its own nerve were removed from cats anesthetized with sodium pentobarbital and placed in an air gap system; the carotid body was bathed in modified Locke's solution equilibrated with 50% O2 in N2, pH 7.43 at 35 degrees C. The sensory discharges, changes in "resting" receptor polarization and the mass receptor potential evoked by ACh or NaCN were recorded with nonpolarizable electrodes placed across the gap. Receptor potentials and sensory discharges evoked by ACh showed an appreciable increase in amplitude and frequency when the preparation was bathed in eserinized Locke. Eserine did not change appreciably the responses evoked by NaCN. Excessive depolarization elicited by either ACh or NaCN was accompanied by sensory discharge block. Removal of K+ ions from the bathing solution induced receptor hyperpolarization and an increase in the amplitude of the evoked receptor potentials. An increase of K+ concentration had the opposite effect. Reduction of Na+ or NaCl to one half, or total removal of this salt, induced an initial reduction and later disappearance of the sensory discharges, some receptor hyperpolarization and a reduction in the amplitude of the evoked receptor potential. Reduction or removal of Ca++ produced receptor depolarization, a marked depression of the evoked receptor potentials, an increase in the frequency of the sensory discharges and a reduction in the amplitude of the nerve action potentials. High Ca++ or Mg++ had little or no effect on action potential amplitude or resting polarization, but decreased sensory discharge frequency and the evoked receptor potentials. Total or partial replacement of Ca++ with Mg++ induced complex effects: (1) receptor depolarization which occurred in low Ca++, was prevented by addition of Mg++ ions; (2) the amplitude of the evoked receptor potentials was depressed; (3) the nerve discharge frequency was reduced as it was in high Mg++ solutions; and (4) the amplitude of the nerve action potentials was reduced as it was in low Ca++ solutions. Temperature had a marked effect on the chemoreceptors since at high temperatures the receptors were depolarized and the discharge frequency increased. The baseline discharge and responses evoked by ACh or NaCN were depressed at low temperatures. The results are discussed in terms of possible receptor mechanisms influenced by the different ions.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D002344:Carotid Body / Q000187:drug effects*; D002415:Cats; D003486:Cyanides / Q000494:pharmacology; D005071:Evoked Potentials / Q000187:drug effects; D066298:In Vitro Techniques; D008274:Magnesium / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects*; D010830:Physostigmine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D011930:Reaction Time / Q000187:drug effects; D012964:Sodium / Q000494:pharmacology; D013696:Temperature
D003486:Cyanides; D012964:Sodium; D010830:Physostigmine; D008274:Magnesium; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium