INTERACTION OF NICOTINE AND A H-2-RECEPTOR ANTAGONIST, FAMOTIDINE, ONGASTRIN AND CHROMOGRANIN-A EXPRESSION

The purpose of this study is to examine the effect of nicotine on famo tidine-induced hypergastrinemia in the rat. In addition, the effects o f nicotine on gene expression for gastrin and chromogranin A (CGA) in the stomach were examined. Famotidine treatment alone (20 mg/kg, 2X/da y 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, nico tine potentiated the hypergastrinemic action of famotidine. The hypega strinemic action of nicotine was not mediated by a downregulation of s tomach somatostatin (SRIF) since stomach SRIF mRNA levels were unaffec ted by nicotine treatment. Administration of nicotine and famotidine a lso upregulated stomach CGA gene expression (i.e., mRNA and protein le vels) significantly. (C) 1997 Elsevier B.V.