Transport of rubidium and sodium in pancreatic islets

Abstract

1. Fluxes of ⁸⁶Rb⁺ and ²²Na⁺ were measured in pancreatic islets of ob/ob-mice. The islets, which contain more than 90% β-cells, were incubated at 37° C in Krebs—Ringer bicarbonate buffer with modifications known to influence insulin release.

2. In the presence of Na⁺, the islets vigorously accumulated Rb⁺. The Rb⁺ uptake was inhibited by depletion of islet Na⁺ or by 1 mm ouabain or 0·1 mm chloromercuribenzene-p-sulphonic acid. Rb⁺ uptake was stimulated by 1 mm-5,5′-dithiobis (2-nitrobenzoic acid) or by depletion of islet Ca²⁺, while 20 mm glucose, 5 mm theophylline, 0·1 mm iodoacetamide, or 1 mm-6,6′-dithionicotinic acid had no significant effects.

3. The efflux of Rb⁺ from preloaded islets followed exponential kinetics with a half-life of about 16 min. The rate of efflux was enhanced by 0·1 mm chloromercuribenzene-p-sulphonic acid and inhibited by 20 mm glucose. Omission of Na⁺, K⁺ or Ca²⁺ from the incubation medium had no significant effects.

4. The efflux of ²²Na⁺ from islets preloaded with this isotope was enhanced by 0·1 mm chloromercuribenzene-p-sulphonic acid or by Ca²⁺ deficiency. It was inhibited by 1 mm ouabain, 0·1 mm-2,4-dinitrophenol, or by omission of Na⁺ from the incubation medium. Omission of K⁺ or the addition of 20 mm glucose had no significant effects.

5. It is concluded that the β-cells are permeable to Na⁺ and Rb⁺ and expel Na⁺ by an active mechanism similar to, or identical with, the Na⁺/K⁺-pump in other cells. The mechanisms of active and passive cation movements are discussed in relation to current hypotheses of stimulus-secretion coupling in the β-cells depending on interactions between Na⁺ and Ca²⁺. In particular, the results support the hypotheses of insulin release being stimulated by ouabain through inhibition of the Na⁺/K⁺-pump and by organic mercurials through enhancement of membrane permeability to cations.

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