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Effects of catecholamines, ATP and ionophore A23187 on potassium and calcium movements in isolated hepatocytes

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Abstract

IN addition to their well known effects on hepatic gluconeogenesis and glycogenolysis, adrenaline and noradrenaline cause a transient net loss of potassium from the liver of many species1. Studies with guinea pig and rabbit liver slices have shown this to be a consequence of a predominantly α -adrenoceptor-mediated increase in the potassium permeability (PK) of the hepatocyte membrane2–4. It has recently become possible to isolate hepatocytes in high yield and with cation levels and metabolic capabilities superior to those of slices, and approaching that of the intact tissue5. We have now confirmed that the effects of catecholamines on potassium movement can be shown with such cells, and we have obtained evidence to support the suggestion that the potassium loss which follows α-adrenoceptor activation in guinea pig liver cells is a consequence of an increase in potassium permeability triggered by a rise in intracellular calcium. The mechanism can be blocked by quinine, as in human erythrocytes19 and barnacle photoreceptors20.

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BURGESS, G., CLARET, M. & JENKINSON, D. Effects of catecholamines, ATP and ionophore A23187 on potassium and calcium movements in isolated hepatocytes. Nature 279, 544–546 (1979). https://doi.org/10.1038/279544a0

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