Abstract

The effects of 24 mM K+ upon the dynamics of immunoreactive insulin (IRI) release were studied in perifused rat islets in the absence of glucose and in its presence at concentrations of 50 and 300 mg. per 100 ml. Raising external K+ to 24 mM in the absence or in the presence of glucose (50 mg. per 100 ml.) was rapidly followed by a transient discharge of IRI. This rapid secretory phase was markedly inhibited in a medium containing 1 mM Na+ and was totally obliterated in a Ca2+-free medium. The early IRI response to a simultaneous increase of glucose to 300 mg. per 100 ml. and of K+ to 24 mM was enhanced while the late response was not significantly modified. In contrast, the same rise in glucose concentration after a twenty-five minute perifusion in a medium containing 24 mM K+ provoked markedly diminished early and late phases of IRI release. Under both experimental conditions, the effect of glucose was almost completely abolished in a medium containing 1 mM Na+. The stimulant action of glucose was not restored when K+ concentration was lowered from 24 to 6 mM at the time of glucose increase, but was normal if this diminution of K+ occurred ten minutes earlier. It is hypothesized that modifications in IRI secretion rate induced by 24 mM K+ result from changes in membrane permeability for Ca2+.

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