ISSN:
1432-1424
Keywords:
Na+, K+-ATPase
;
Ca2+-activated K+ permeability
;
ouabain
;
quinine
;
pancreatic B-cell
;
insulin release
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Chemistry and Pharmacology
Notes:
Summary A rise in the extracellular concentration of glucose from an intermediate to a high value changes the burst pattern of electrical activity of the pancreatic B-cell into a continuous firing, and yet activates the B-cell Ca2+-sensitive K+ permeability. The hypothesis that glucose exerts such effects by inhibiting the Na+, K+-ATPase was investigated. Ouabain (1 mM) mimicked the effect of 16.7mm glucose in stimulating86Rb,45Ca outflow and insulin release from perifused rat pancreatic islets first exposed to 8.3mm glucose. The stimulation by ouabain of86Rb outflow was reduced in the absence of extracellular Ca2+ and almost completely abolished in the presence of quinine, and inhibitor of the Ca2+-sensitive K+ permeability. In the presence of ouabain, a rise in the glucose concentration from 8.3 to 16.7mm failed to stimulate86Rb outflow. However, the rise in the glucose concentration failed to inhibit86Rb influx in islet cells, while ouabain dramatically reduced86Rb influx whether in the presence of 8.3 or 16.7mm glucose. These findings do not suggest that inhibition of the B-cell Na+, K+-ATPase represents the mechanism by which glucose in high concentration stimulates86Rb outflow and induces continous electrical activity in the B-cell.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF01870596
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