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Activation of cell membrane potassium conductance by mercury in cultured renal epitheloid (MDCK) cells
Author(s) -
Jungwirth A.,
Ritter M.,
Paulmichl M.,
Lang F.
Publication year - 1991
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041460105
Subject(s) - chemistry , intracellular , extracellular , biophysics , cell membrane , membrane potential , potassium , hyperpolarization (physics) , depolarization , calcium , pertussis toxin , membrane , cholera toxin , biochemistry , biology , endocrinology , stereochemistry , g protein , signal transduction , organic chemistry , nuclear magnetic resonance spectroscopy
To elucidate mechanisms of mercury toxicity, the cell membrane potential has been determined continuously in cultured kidney (MDCK)‐cells during reversible application of mercury ions to extracellular perfusate. Exposure of the cells to 1μM mercury ions is followed by rapid, sustained, and slowly reversible hyperpolarization of the cell membrane, increase of cell membrane potassium selectivity, and decrease of cell membrane resistance. Thus, mercury ions enhance the potassium conductance of the cell membrane. Half maximal hyperpolarizing effect is elicited by ≈0.2 μM. Higher concentrations of mercury ions (> 10 μM) eventually depolarize the cell membrane. At extracellular calcium activity reduced to less than 0.1 μM, 1 μM mercury ions still leads to a sustained hyperpolarization and increase of potassium selectivity of the cell membrane. As evident from fluorescence measurements, 10 μM, but not 1 μM mercury ions leads to a rapid increase of intracellular calcium activity. Pretreatment of the cells with either pertussis toxin or cholera toxin does not blunt the hyperpolarizing effect of mercury ions. In conclusion, mercury ions activate the potassium conductance by a mechanism independent of increase of intracellular calcium activity and of cholera toxin‐or pertussis toxin‐sensitive G‐proteins. This activation of potassium conductance may account for early effects of mercury intoxication, such as kaliuresis.

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