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PubMed1989

Does glucose decrease cytosolic free calcium in normal pancreatic islet cells?

Cytosolic free Ca2+ concentration ([Ca2+]i) was measured in normal rat pancreatic islet cells using the intracellular Ca2+ indicator fura 2. Glucose induced an initial decrease followed by a secondary rise in [Ca2+]i. The secondary rise probably resulted from an increase in Ca2+ inflow into the cells, while the initial decrease displayed several characteristics of the well known initial decrease in 45Ca efflux induced by glucose in prelabelled pancreatic islets. It is concluded that glucose may exert both an inhibitory and a stimulatory effect on [Ca2+]i in normal isolated islet cells.

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Effects of verapamil and nifedipine on gliclazide-induced increase in cytosolic free Ca2+ in pancreatic islet cells.

The changes in cytosolic free calcium [Ca2+]i induced by the sulfonylurea gliclazide and potassium in normal rat pancreatic islet cells were measured using the fluorescent Ca2+ indicator fura-2. Both in the absence or presence of 5.6 mM glucose, gliclazide caused a rapid and sustained increase in [Ca2+]i. The phenylalkylamine verapamil reduced these increases, but the Ca2+ channel blocker was more potent in the presence than in the absence of glucose. In contrast, nifedipine, a Ca2+ channel blocker of another chemical type, reduced to a similar extent the increase in [Ca2+]i evoked by gliclazide in the absence and presence of glucose. In the absence of glucose, a rise in extracellular K+ concentration from 5 to 20 or 30 mM also induced a rapid and sustained rise in [Ca2+]i. Verapamil more markedly reduced the rise in [Ca2+]i induced by 30 mM than by 20 mM K+. It is concluded that gliclazide increases Ca2+ inflow into normal islet cells primarily, if not exclusively, by opening voltage-sensitive Ca2+ channels. The differential sensitivity toward verapamil of gliclazide-induced rise in [Ca2+]i can be explained by the use-dependent block exerted by Ca2+ channel blockers of the phenylalkylamine type.

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