Summary
Administration of potassium chloride to normal rats causes a decrease in the hyperglycemic response to diazoxide.
The hyperglycemic effect of diazoxide has been shown to exaggerate in animals with progressively increasing negative potassium balance.
Potassium deficiency results in a decrease in intracellular potassium concentration accompanied by an increase in intracellular sodium concentration.
There is no influence of varying potassium and sodium concentrations on 3′,5′-AMP phosphodiesterase activity.
The activity of phosphorylase phosphatase has been found progressively reduced with increasing sodium concentration in the incubate.
Diazoxide administered in doses insufficient to increase phosphorylase activity in normal rats has been shown to gain such action in rats with potassium deficiency.
These data indicate the increase in the hyperglycemic action of diazoxide in potassium deficiency being caused by a reduction in phosphorylase phosphatase activity in consequence of the increase in intracellular sodium concentration.
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Ein Teil der Ergebnisse wurde auf der 29. Tagung der Deutschen Pharmakologischen Gesellschaft vorgetragen (Kaess, Losert, Schultz, Senft u. Sitt, 1966).
Wir danken der Deutschen Forschungsgemeinschaft für die Unterstützung unserer Arbeiten.
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Kaess, H., Senft, G., Losert, W. et al. Mechanismus der gesteigerten glykogenolytischen Wirkung des Diazoxids im Kaliummangel. Naunyn - Schmiedebergs Arch 253, 395–401 (1966). https://doi.org/10.1007/BF00245978
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DOI: https://doi.org/10.1007/BF00245978