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Glucose stimulation of ouabain‐resistant efflux of Na+ from rat pancreatic islets.
Author(s) -
Ali L,
Hellman B
Publication year - 1991
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1991.sp018511
Subject(s) - ouabain , chemistry , medicine , bumetanide , sodium , endocrinology , pancreatic islets , amiloride , stimulation , efflux , extracellular , islet , insulin , biochemistry , biology , cotransporter , organic chemistry
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.