Premium
Mechanism of the effect of cyanide on cell membrane potentials in Necturus gall‐bladder epithelium.
Author(s) -
BelloReuss E,
Grady T P,
Reuss L
Publication year - 1981
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 - 10.1113/jphysiol.1981.sp013712
Subject(s) - hyperpolarization (physics) , necturus , potassium , chemistry , biophysics , cyanide , membrane potential , calcium , intracellular , biochemistry , cell membrane , membrane , ionophore , sodium , potassium cyanide , membrane permeability , apical membrane , biology , inorganic chemistry , stereochemistry , organic chemistry , nuclear magnetic resonance spectroscopy
1. Addition of sodium cyanide to the mucosal or the serosal medium bathing the isolated gall‐bladder of Necturus maculosus causes hyperpolarization of both apical and basolateral membrane of the epithelial cells. The effect of cyanide is practically immediate, reversible (if exposure is brief), and long‐lasting (greater than 30 min). 2. The hyperpolarization is accompanied by: (a) reduction of the equivalent resistance of the cell membranes, as shown by cable analysis and input resistance measurements, and (b) increase of the potassium selectivity of both cell membranes, as evidenced by the effects of external substitutions of potassium for sodium on cell membrane potentials. We conclude that the cyanide‐induced hyperpolarization is caused mainly or exclusively by an increase of the potassium permeability of the cell membranes. 3. Addition of the calcium ionophore A23187 (5 microM) to the mucosal medium in the presence of 1 mM‐calcium caused similar effects to those produced by cyanide. After either cyanide or A23187, addition of the other agent did not cause further membrane potential changes. 4. Quinine (100 microM, mucosal medium) reduced the potassium permeability of the apical membrane both under control conditions and during exposure to cyanide. 5. We suggest that the cyanide‐induced increase of the potassium permeability of the cell membrane is mediated by an elevation of intracellular calcium ion activity, attributable to release from mitochondrial sources.