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AJP - Gastrointestinal and Liver Physiology, Vol 264, Issue 1 137-G142, Copyright © 1993 by American Physiological Society
ARTICLES |
K. W. Gasser and J. R. Holda
Department of Biological Sciences, Northern Illinois University, DeKalb 60115-2861.
Electrolyte transport pathways in the pancreatic secretory granules may contribute to acini fluid production after fusion with the apical membrane. A component of this granule transport is a K(+)-selective pathway that has been measured indirectly by ionophore-induced lysis of the isolated secretory granules when suspended in a KCl solution. This granule membrane K+ transport was shown to be inhibited by physiological levels of ATP in a dose-dependent manner and was not reversed by ADP. The sulfonylurea tolbutamide (0.5 mM), a recognized inhibitor of ATP-sensitive K+ channels, also reduced the ionophore-dependent lysis by 46%. The ATP sensitivity of the K+ transport was influenced by pH (increased ATP sensitivity with decreasing pH) and KCl concentration (increased ATP sensitivity with increasing KCl). In addition, preincubation with phospholipase A2 (8.3 x 10(-10) g/ml) or lysophospholipids (6.7 x 10(-7) g/ml) produced a significant decrease in the granule K+ transport. However, it is not likely that this inhibition is due to a change in membrane fluidity, because fluidization with arachidonic acid or octanol did not have a comparable effect. The results then support a granule-associated K+ transport in pancreatic acinar cells and suggest that it is ATP and lysophospholipid sensitive.
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