Experimental Physiology
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Quarterly Journal of Experimental Physiology 69.4 pp 831-839
© The Physiological Society 1984
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ELECTROPHYSIOLOGICAL EVIDENCE FOR THE INHIBITION OF POTASSIUM PERMEABILITY IN PANCREATIC beta-CELLS BY GLIBENCLAMIDE

Rosa Ferrer 1, Illani Atwater 1, P. C. Croghan 1, E. Rojas 1, E. M. Omer 2, and A. A. Gonçalves 3

1 Department of Biophysics, School of Biological Sciences, University of East Anglia, Norwich NR4 7TJ
2 Department of Internal Medicine, West Norwich Hospital, Norwich, NR2 3TU
3 Departamento de Fisiologia e Biofisica, Universidade Estadual de Campinas (UNICAMP), 13100 Campinas, So Paulo, Brazil

The effects of glibenclamide on the electrical activity of the beta-cells of the islets of Langerhans of normal mice have been investigated in the absence and presence of glucose (11·1 mM). Glibenclamide depolarized the cell membrane and this has been interpreted in terms of an increase in the ratio of the Na+ and K+ permeabilities, PNa/ PK. This ratio increased from 0·05 to 0·24 in the presence of 4 µM glibenclamide and zero glucose. The input resistance of the beta-cells also increased. These observations indicate a decrease in K+ permeability. The effect is only slowly reversed after removal of glibenclamide. Uncouplers of oxidative phosphorylation do not reverse the depolarization induced by glibenclamide. It is suggested that glibenclamide is acting directly to inhibit the [Ca2+]i-gated K+ permeability in the beta-cell membrane.

Submitted on September 20, 1983




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J.-C. Henquin
A Minimum of Fuel Is Necessary for Tolbutamide to Mimic the Effects of Glucose on Electrical Activity in Pancreatic {beta}-Cells
Endocrinology, March 1, 1998; 139(3): 993 - 998.
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