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Effect of K+ deprivation and ouabain upon glucagon release.

The effects of K+ depletion and ouabain (0.1, 0.5, and 1 mM) on glucagon and insulin release from the in vitro perfused rat pancreas were studied in the absence or presence of arginine (10 mM). In the absence of arginine, K+ depletion resulted in an inhibition of glucagon release, both at a low (2.8 mM) and a higher (8.3 mM) concentration of glucose, whereas ouabain enhanced glucagon secretion. In the presence of arginine, K+ deprivation induced limited and short lived oscillations in the rate of glucagon release at both low and high glucose levels. In the presence of arginine, ouabain induced first a short lived stimulation and, thereafter, a severe and sustained inhibition of glucagon release. The restoration of the normal K+ concentration or the removal of ouabain was followed by a marked and transient inhibition of glucagon release which was most prominent in the presence of arginine. In agreement with previous investigations, K+ deprivation or ouabain facilitated insulin release evoked by glucose and/or arginine. The results suggest that a primary alteration in K+ availability and/or transport affects in a dual manner the release of glucagon, depending on environmental factors such as the type of stimulus used to activate the secretory process.