1. Fluxes of (86)Rb(+) and (22)Na(+) were measured in pancreatic islets of ob/ob-mice. The islets, which contain more than 90% beta-cells, were incubated at 37 degrees 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 Ca(2+), 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 Ca(2+) from the incubation medium had no significant effects.4. The efflux of (22)Na(+) from islets preloaded with this isotope was enhanced by 0.1 mm chloromercuribenzene-p-sulphonic acid or by Ca(2+) 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 beta-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 beta-cells depending on interactions between Na(+) and Ca(2+). 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.