Opposite effects of intracellular Ca²⁺ and glucose on K⁺ permeability of pancreatic islet cells

Abstract

MANY cells possess a potassium permeability system that is activated by an increase in the concentration of Ca²⁺ in the cytosol. This Ca²⁺-sensitive permeability was originally described¹ and is best characterised² in erythrocytes, where its function is still not known. However, a similar mechanism could represent a physiological control of the membrane conductance in excitable tissues such as nerve^3,4 or cardiac muscle⁵. Physiological stimulation of salivary glands results in a Ca²⁺-mediated release of potassium⁶ and hyperpolarisation⁷. In contrast, glucose depolarises pancreatic B cells^8,9 by decreasing their potassium permeability^10,11, but also stimulates Ca²⁺ uptake by islet cells^12–14. I report here an investigation into the possible interplay between these two effects of glucose. Evidence that intracellular Ca²⁺ increases the K⁺ permeability in pancreatic islet cells and that the glucose-stimulated Ca²⁺ inflow may represent a feedback control of the glucose-mediated decrease in K⁺ permeability of B cells is presented.