Glucose stimulation of ouabain‐resistant efflux of Na+ from rat pancreatic islets.

1. Integrating flame photometry was employed for measuring the mobilization of sodium from rat pancreatic islets after substitution of extracellular Na+ by N‐methylglucamine. 2. Glucose accelerated the initial loss of sodium both in the absence and presence of ouabain (1 mM). In the latter case the effect was maximal at 5 mM of the sugar. 3. Amiloride (0.1 mM), an inhibitor of Na(+)‐H+ exchange, prevented the effect of glucose on the ouabain‐resistant Na+ efflux, increasing the rate of outward transport in the absence of the sugar. 4. Extracellular K+ and arginine (10 mM) mimicked the action of glucose in promoting a ouabain‐resistant mobilization of sodium. 5. Whereas the hypoglycaemic sulphonylurea tolbutamide (100 microM) did not modify the outward transport of Na+, the ouabain‐resistant component of this process was partially suppressed after bumetanide (100 microM) inhibition of the chloride‐dependent co‐transport of Na+ and K+. 6. It is suggested that the glucose‐induced lowering of the steady‐state content of islet sodium involves an increased outward transport mediated at least in part by mechanisms other than stimulation of the Na(+)‐K+ pump.