PMID: 9178349Mar 26, 1997Paper

Interaction of nicotine and a H2-receptor antagonist, famotidine, on gastrin and chromogranin A expression

Regulatory Peptides
G GomezG H Greeley

Abstract

The purpose of this study is to examine the effect of nicotine on famotidine-induced hypergastrinemia in the rat. In addition, the effects of nicotine on gene expression for gastrin and chromogranin A (CGA) in the stomach were examined. Famotidine treatment alone (20 mg/kg. 2 x/day for 14 days) increased serum gastrin levels significantly (P < 0.05) but not antral levels of gastrin mRNA and peptide. Nicotine treatment (12 mg/kg/d) alone did not affect serum gastrin levels; however, nicotine potentiated the hypergastrinemic action of famotidine. The hypergastrinemic action of nicotine was not mediated by a downregulation of stomach somatostatin (SRIF) since stomach SRIF mRNA levels were unaffected by nicotine treatment. Administration of nicotine and famotidine also upregulated stomach CGA gene expression (i.e., mRNA and protein levels) significantly.

References

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Citations

Aug 25, 2011·Endocrine Reviews·Alessandro BartolomucciStephen R J Salton
Jun 17, 2015·Experimental Physiology·Soad Shaker AliMansour Ibrahem Suliman

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