The Effect of Potassium and Valinomycin on Insulin and Grlucagon Secretion in the Perfused Rat Pancreas*

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Abstract
The response of the .alpha.- and .beta.-cells of the perfused rat pancreas to an elevation of K ion concentration and to the K ionophore, valinomycin (1 .times. 10-6 M) was examined. Elevation of K from a baseline concentration of 5.8 mM to 11.3, 18.3 and 53.3 mM caused a biphasic release of immunoreactive insulin characterized by a spiked 1st phase and a low sustained 2nd phase and a spiked release of immunoreactive glucagon followed by a very low sustained secretion that ended with the termination of the stimulation. The 2nd phase of K-stimulated insulin release increased in the presence of basal glucose (3.3 mM). Sequential higher concentrations of K caused a dose-response increase in both phases of insulin release, but did not increase glucagon secretion. Valinomycin inhibited the insulin secretion caused by K, arginine and glucose and the glucagon secretion caused by K and arginine, K, when applied on the 2nd phase of arginine-stimulated insulin and glucagon release, enhanced the secretion of insulin but caused a dramatic inhibition of glucagon that did not correlate directly with insulin release and which may possibly result from the entrance of an excessive amount of Ca into the islet cells. The secretion caused by K was attributed to its depolarizing qualities. If the principal effect of valinomycin is a result of its postulated hyperpolarization of the islet cells, it seems that the electrical behavior of the .alpha. and .beta.-cells with regard to secretion is similar; depolarization enhances secretion and hyperpolarization inhibits it. The established inhibition of glucagon secretion by glucose must be induced by a mechanism other than depolarization.