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Na + pump inhibition and non‐selective cation channel activation by cyanide and anoxia in guinea‐pig chromaffin cells
Author(s) -
Inoue M.,
Fujishiro N.,
Imanaga I.
Publication year - 1999
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1999.0385m.x
Subject(s) - depolarization , chemistry , reversal potential , biophysics , membrane potential , ouabain , cyanide , hyperpolarization (physics) , patch clamp , medicine , endocrinology , biochemistry , stereochemistry , biology , sodium , inorganic chemistry , receptor , organic chemistry , nuclear magnetic resonance spectroscopy
1 Hypoxia and metabolic inhibition with cyanide (CN) evoke catecholamine secretion in adrenal chromaffin cells through depolarization. We elucidated mechanisms for a CN‐ or anoxia‐induced inward (depolarization) current, using the perforated patch method. 2 Bath application of Ba 2+ induced a dose‐dependent inhibition of a muscarine‐induced current (I MUS ) and part of the CN‐induced current (I CN ) with an IC 50 (concentration responsible for 50 % inhibition) of 1.3 mM. The Ba 2+ ‐sensitive component was estimated to comprise 58 % of the total I CN . 3 The Ba 2+ ‐resistant component of I CN tended to increase with shifts of membrane potential from ‐40 to 40 mV and was markedly suppressed by exposure to a K + ‐free solution or 200 μ m ouabain, indicating that the majority of the Ba 2+ ‐resistant component of I CN is due to suppression of the Na + pump current (I pump ). 4 The non‐ I pump component of I CN diminished progressively in K + ‐free solution. Substitution of glucose for sucrose in a K + ‐free CN solution further diminished the CN potency to produce the non‐ I pump component. 5 The I‐V relationship for the non‐ I pump component of I CN had a reversal potential of ‐3 and ‐47 mV at 147 and 5.5 mM Na + , respectively, and showed an outward rectification, indicating that the non‐ I pump component of I CN is due to activation of non‐selective cation channels. 6 Exposure to anoxia induced a current with an amplitude comparable to that of I CN , and the anoxia‐induced current apparently occluded development of I CN . The anoxia‐induced current diminished by ca 60 % in the absence of K + and reversed polarity at 5 mV under K + ‐free conditions. 5 It is concluded that exposure to CN and to anoxia induces suppression of the Na + pump and activation of non‐selective cation channels, probably due to an ATP decrease resulting mainly from consumption by the Na + pump.