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.[1]References
- Glucose stimulation of ouabain-resistant efflux of Na+ from rat pancreatic islets. Ali, L., Hellman, B. J. Physiol. (Lond.) (1991) [Pubmed]
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