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. 1984 Nov;83(3):831–839. doi: 10.1111/j.1476-5381.1984.tb16239.x

Efflux of 86Rb from rat and mouse pancreatic islets: the role of membrane depolarization.

E K Matthews, P A Shotton
PMCID: PMC1987071  PMID: 6391599

Abstract

The efflux of 86Rb from rat or mouse perifused islets preloaded with the isotope has been used as an index of the potassium permeability of the islet beta-cell membrane. Cellular transmembrane potentials were altered by changing [K]O or by direct electrical stimulation and the effects on potassium permeability examined. Omission of KCl from the medium perifusing rat islets induced a biphasic change in 86Rb efflux, a brief decline being superseded by a pronounced increase in efflux. Re-introduction of KCl, 4.7 mM, caused a further increase in 86Rb efflux preceding a return to control values. Increasing [K]O from 4.7 mM to 10 mM, 20 mM or 47 mM caused a phasic increase in 86Rb efflux with the magnitude of both the peak and average rate of efflux being dependent upon the extent of the change in [K]O. The increase in 86Rb efflux produced by [K]O, 47 mM, was attenuated by Co2+, 2.56 mM (51% inhibition) or quinine, 10 microM (47% inhibition), but efflux remained significantly (P less than 0.001) above control values. Electrical stimulation of single microdissected mouse pancreatic islets by currents of 0.1 to 0.5 mA evoked a rapid, phasic increase in 86Rb efflux. The magnitude of the response was unaffected by EGTA, 2 mM, or nupercaine, 100 microM. These observations are discussed in relation to the mechanisms controlling the potassium permeability, membrane potential and insulin secretion of the pancreatic islet beta-cell.(ABSTRACT TRUNCATED AT 250 WORDS)

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Selected References

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