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Effect of Platelet-Activating Factor on Gastrin Release from Cultured Rabbit G-Cells

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Abstract

Gastric infection with Helicobacter pylori is associated with hypergastrinemia. Platelet activating factor (PAF) is produced in H. pylori-infected mucosa. The effects of PAF on gastrin release from cultured antral rabbit G cells were examined. Rabbit antral G-cells were obtained by collagenase-EDTA digestion and enriched by centrifugal elutriation. After 40 hr in culture, gastrin release in response to PAF was assessed. PAF stimulated gastrin release in a dose-dependent manner. A maximal release of 67% above basal was seen with PAF at 100 nM. PAF also enhanced the gastrin release stimulated by forskolin and bombesin. PAF-stimulated gastrin release was abolished by a PAF-receptor antagonist. Gastrin release stimulated by PAF was abolished by chelation of intra- or extracellular calcium or the L-type calcium channel inhibitor verapamil as well as by the protein kinase C inhibitor chelerythrine. Platelet-activating factor may contribute to the hypergastrinemia of H. pylori infection by stimulating gastrin release from G cells. PAF-stimulated gastrin release involves influx of extracellular calcium via L-type channels and activation of protein kinase C.

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Beales, I.L. Effect of Platelet-Activating Factor on Gastrin Release from Cultured Rabbit G-Cells. Dig Dis Sci 46, 301–306 (2001). https://doi.org/10.1023/A:1005553722093

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