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

Guillermo Gomez, Vidyavathi Udupi, George H. Greeley

Research output: Contribution to journalArticle

3 Scopus citations

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, 2x/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.

Original languageEnglish (US)
Pages (from-to)77-82
Number of pages6
JournalRegulatory Peptides
Volume69
Issue number2
DOIs
StatePublished - Mar 26 1997

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Keywords

  • CGA
  • Gut
  • Peptides

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Endocrinology
  • Clinical Biochemistry
  • Cellular and Molecular Neuroscience

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